A closer look at 'autoimmune diseases'

Is the body really 'attacking itself'?

Disclaimer: nothing in this article is to be taken as medical advice. The information provided here is to be used purely for informational and educational purposes.

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An ‘auto-immune disease’ is defined as “a condition in which the body's immune system mistakes its own healthy tissues as foreign and attacks them.” According to the NIH, there are more than 80 such conditions recognised. Examples include type 1 diabetes, rheumatoid arthritis, psoriasis, Inflammatory Bowel Disease (IBS), Crohn’s disease, Lupus, multiple sclerosis (MS), Hashimoto's thyroiditis and Coeliac disease.

Most of these diseases are said to be incurable, requiring life-long treatment. Globally, the incidence rate is on the rise. As of 2018, the British Society for Immunology estimates that the growth rate in the UK “ranges between 3% and 9% year on year”. Since 2011, global expenditure for treatments has increased from $23b to $141b per annum, and is showing no sign of slowing down. As of 2021, 4.5% of the global population is said to be affected.

What’s behind the rise? According to the NIH; “autoimmune diseases are affecting more people for reasons unknown. Likewise, the causes of these diseases remain a mystery”. Vague allusions to ‘genetic’ and ‘environmental factors’ are often put forward as explanations. With regards to the ‘genetic’ hypothesis, James Lee of the Francis Crick Institute notes that “human genetics hasn’t altered over the past few decades … so something must be changing in the outside world in a way that is increasing our predisposition to autoimmune disease”. This leaves the ‘environmental factors’ explanation. One such factor is said to be the ‘Western diet’, although it is unclear why this would affect places like Nigeria, India, or Japan.

The history of ‘auto-immune diseases’

Prior to the 1950s, the prevailing view was that of ‘horror autotoxicus’ – ‘fear of self-toxicity’ – a term coined by German scientist Paul Ehrlich. Ehrlich conducted experiments in which “rabbits, goats, and other animals were injected with the blood of another species or the blood of the same species. They found that individuals injected with a different species’ blood formed antibodies against the foreign cells, while those injected with the same species’ blood didn’t form disease-causing autoantibodies.” Thus, Ehrlich held the position that ‘auto-immune diseases’ are an impossibility.

This changed in the 1950s, when Noel Rose carried out a series of experiments using thyroglobulin, a protein found in the thyroid gland; “[he] extracted small amounts of thyroglobulin from living rabbits, then devised innovative methods to inject the protein back into the same animals … to his surprise, he discovered that the rabbits produced antibodies to fight off the invading antigen, even though it was derived from their own bodies.” Rose is widely regarded as the ‘father of autoimmunity’, and it would appear that it is these experiments, that form the basis for the claim that Ehrlich was wrong, and that the body can, in fact, ‘attack itself’.

Some 40 years earlier, in 1913, French scientist Charles Richet was awarded the Nobel prize for his discovery of ‘anaphylaxis’; “a severe and potentially life-threatening reaction to a trigger such as an allergy”. In his acceptance speech, Richet explains how “a subject that has received a poison” will react, when the same poison is re-administered a few days later. According to him, there are three possibilities:

1.) The individual reacts in the same way as previously.

2.) The individual has become less sensitive – in other words, they will have developed some form of ‘immunity’, also known as ‘mithridatism’ – defined as “tolerance to a poison acquired by taking gradually increased doses of it”. Richet uses the example of morphine injections. A similar phenomenon seems to apply in the field of psychology.

3.) The individual has become more sensitive; “the first injection, instead of protecting the organism, renders it more fragile and more susceptible”. This is what Richet called ‘anaphylaxis’.

Richet and others observed this phenomenon after injecting various substances that included “milk, serum, egg” and “muscle extract” into various animals. He noted that “proteins without exception produce anaphylaxis”, and that “we are so constituted that we can never receive other proteins into the blood than those that have been modified by digestive juices”, therefore implying that injecting proteins into the bloodstream (as is done, for example, with ‘vaccination’), can lead, in some cases to this “heightened sensitivity”. Anaphylaxis, according to Richet; “is necessary to the species, often to the detriment of the individual … [as it] defends the species against the peril of adulteration.”

These reactions, according to extensive experiments carried out by Rosenau and Anderson in 1909, are not always immediate or predictable. Sometimes, death occurs almost instantly. Sometimes, ‘severe’ or ‘very severe’ symptoms are experienced. According to Richet, these discrepancies are due to the fact that “every living being, though presenting the strongest resemblances to others of his species, has his own characteristics so that he is himself and not somebody else”.

It would appear that Rose’s findings are consistent with those of Richet and others; injecting protein into the blood stream, can lead to deleterious effects. It is unclear then, why the results of his experiments would lead to the hypothesis that the body can ‘attack itself’. But let’s say Rose is correct, we are still left with the all-important question; why does it happen?

To answer this, let’s take a closer look at one such disease; ‘multiple sclerosis’.

Multiple sclerosis

Multiple sclerosis “is one of the most common diseases of the nervous system, afflicting people of virtually all ages around the world, although it has a special preference for young people, especially women, and for those who grew up in northern latitudes.”

Symptoms are said to usually include “sudden neurologic symptoms including vision loss, paralysis, numbness, and walking difficulties”. This is said to happen because the body mistakenly ‘attacks’ the ‘myelin sheath’ found in the brain and spinal cord. The sheath is an insulating layer that surrounds ‘axons’ – a sort of electric cable that connects neurons, and allows electrical signals to be transmitted throughout the body. It is created by ‘oligodendrocytes’ in the ‘central nervous system’ (CNS – the brain and spinal cord), and ‘Schwann cells’ in the ‘peripheral nervous system’ (PNS – nerves that branch out from the brain and spinal cord and extend to other parts of the body), and allows for conduction speed to be vastly increased; “whereas unmyelinated axon conduction velocities range from about 0.5 to 10 m/s, myelinated axons can conduct at velocities up to 150 m/s.”

The body’s ‘attack’ on these sheaths, cause them to become inflamed and create small patches known as ‘plaques’ or ‘lesions’, and this is what is said to cause the aforementioned symptoms. One way to think of this is as a vast network of fibre optic cables, such as those used to provide Internet connectivity. If any of these cables are damaged, the transmission of data may slow down, or stop altogether.

The first “identifiable instance of MS” is said to date back to the early 19th century. At the time; “scientists suspected that some form of toxin or poison caused MS. Because most MS damage occurs around blood vessels, it seemed reasonable that a toxin circulating in the bloodstream leaked out into the brain, even though no researcher could find a trace of it”.

It wasn’t until the 1930s that research led by Rockefeller Institute virologist Thomas Rivers, led to the idea that MS is in fact, an ‘autoimmune disease’; “it had been known that people vaccinated against viral illnesses, especially rabies, sometimes developed a disease resembling MS. It had been assumed that this occurred because the virus in the vaccines was not completely inactivated … by injecting myelin he knew to be virus-free into laboratory animals under the proper conditions, he could induce their immune systems to attack their own myelin, producing a disease very similar to MS”. This ‘model’ – referred to as ‘experimental allergic encephalomyelitis’ is what “paved the way to modern theories of autoimmunity, for it demonstrated how the body can generate an immunologic attack against itself”. Rivers concludes his study by stating that “repeated intramuscular injections of brain extracts and brain emulsions into eight monkeys were followed in two instances by an inflammatory reaction, accompanied by demyelination, in the central nervous system.”

Given that ‘viruses’ are said to be bits of genetic material wrapped inside a protein shell (‘capsid’) such a reaction appears to be consistent with the phenomenon of anaphylaxis described by Richet (and thus, nothing to do with the fact the ‘virus’ was not ‘completely inactivated’). Others seem to have come to similar conclusions; “these complications were widely attributed to an incomplete inactivation of the vaccine virus, which was grown in rabbit brain tissues. But there was another possible explanation: repeated injections of brain tissue might have triggered an allergic reaction”.

It is also worth mentioning the work of another researcher, Hurst, who observed that “the introduction parenterally in rabbits of emulsions of normal brain tissue is followed by severe toxic manifestations leading to wasting and death. In a few cases paralyses occur, but similar nervous symptoms have been encountered in other work not involving the use of brain emulsions”. This is most interesting, given that we’re told that Popper and Landsteiner, and later, Flexner and Lewis, used a similar technique to allegedly prove that a ‘virus’ was the cause of the disease known as ‘polio’ (which is said to be characterised by a unique form of paralysis). In their study, Flexner and Lewis stated that “the material employed for inoculation of two monkeys consisted of the emulsified spinal cord in salt solution obtained from a child nine years old, who died on the fourth day of attack from infantile paralysis. The emulsion was injected into the peritoneal cavity of the monkeys. One of the latter became severely sick on the sixth day and died on the eighth day after inoculation. The other monkey became paralyzed on the seventeenth day and was killed on the nineteenth day after inoculation”.

The experiments carried out by Rivers and Hurst show quite clearly, that the observations made by Popper and Landsteiner, Flexner and Lewis, would have been the result of either:

a.) a form of anaphylaxis, as per Richet’s findings, or;

b.) as Popper and Landsteiner had originally hypothesised, “a transferred poison”

As to what that poison is, it would appear that arsenic and lead, are able to induce the exact same symptoms that are attributed to the ‘virus’ that is said to cause ‘polio’ – and it is perhaps no coincidence given that the original outbreaks started at around the same time that various lead and arsenic based pesticides, began being used en-masse (see here and here). Popper and Landsteiner’s original hypothesis certainly holds some water, when we consider that arsenic nanoparticles are about the same size, as the ‘polio virus’, which is said to have a diameter ranging between 25 and 30nm.

As seems to so often be the case, the experiments that laid the foundations for the idea that the body somehow ‘attacks itself’ spontaneously, is dubious to say the least.

So, let’s look at the ‘environmental factors’.

Environmental factors

As seems to be so often the case, arsenic has been found to directly affect the myelin sheath; “on the pathology of the peripheral nerves in arsenical neuropathy, there are only few and brief reports in the literature. Chhuttani et al. reported the pathological findings in the peripheral nerves of 23 subjects. They found thickening of the perineurium, increased fibrous tissue in the endoneurium and perineurium, reduction in the number of myelinated fibres and degenerative changes of myelin sheaths, as well as reduction and fragmentation of axons”. Similar findings have been reported for lead, thallium and mercury.

High levels of arsenic have also been detected in those suffering from the condition; “the association between arsenic level and oxidative stress parameters supports the hypothesis that high serum arsenic levels may play a critical role in the pathogenesis of MS progression”.

MS is not alone in the regard; arsenic appears to be linked to a great many other ‘autoimmune diseases’. For example, in the case of Hashimoto’s, studies have shown increased levels of arsenic and lead in blood samples compared to controls. The same appears to be the case for psoriasis, where again, “values of As [arsenic] were significantly higher in scalp hair, blood, and urine samples of patients with mild and severe psoriasis as compared to the controls”. Similar findings have been reported for ‘type 1 diabetes’; “analysis of nutrients and metals at community-level indicated that arsenic level was positively associated with type 1 diabetes incidence rate.”

What role does arsenic play in all of this? A few years ago, a grant was given by the NIH to study the role of copper in the development of MS; “one way to study myelin degeneration is to feed a toxin called cuprizone to mice, which promotes the development of MS. Cuprizone binds to copper, and researchers think that very action is toxic, causing copper levels to fall which, possibly, leads to myelin loss”. Copper and zinc are both important components of myelin. Thus, anything that removes or prevents copper or zinc from being used properly, will in turn damage myelin, and lead to the symptoms we are discussing. Researchers found similar symptoms to those of SMON (and MS) in patients suffering from “copper-deficient myelo-neuropathy”, and others have found lower levels of both zinc and copper in MS patients when compared to controls. As per the findings presented here, arsenic has an affinity for such metals, and as a result, will disrupt all kinds of processes.

Like viruses, the idea that the body – an incredibly sophisticated piece of machinery – that even to this day, scientists appear to barely understand – can one day decide to ‘accidentally attack itself’ – is beyond absurd. And like ‘viruses’, such ideas seem to have been put out as a deliberate attempt to muddy the waters, and prevent people from getting to the root of the problem, which like many of the ‘diseases’ we’ve already covered, seems to the widespread dissemination of poisons, in particular arsenic.

If we are to solve the problem of ‘auto immune disease’, perhaps we should abandon the preposterous and foolish notion that the body ‘attacks itself’, and instead focus on working out how we’re going to go about decontaminating our atmosphere and our bodies.

As always, thank you to Caroline for her help in pulling this information together.