Infants are Uniquely Vulnerable to Aluminium in Vaccines

Professor Chris Exley | 9th January 2020 | Infection/Disease, Paediatrics, Pharmacy/Drugs
The Hippocratic Post

Aluminium is Toxic

In 1984, as an undergraduate at the University of Stirling, Scotland and while carrying out my first piece of independent research, I watched for the first time a fish, a salmon parr, die from acute aluminium toxicity. The whole process took less than forty-eight hours. Within six hours, the fish showed signs of distress and its behaviour changed markedly. It proceeded to seek out the corners of the tank, pushing its head and body against the side of the tank. After twenty-four hours, it began to move randomly and chaotically around the tank before losing its orientation, slipping onto its back, taking a last gasp, before dying. I was left in no doubt about the toxicity of aluminium. I am recalling this event herein because there does seem to be significant complacency concerning the toxicity of aluminium.

An Aluminium Adjuvant is Acutely Toxic Too

In a recent post (here) I explained why a single injection of a vaccine that includes an aluminium adjuvant is, akin to the salmon above, also an acute exposure to aluminium. It is acute because the total concentration of aluminium in the immediate vicinity of the injection site is extremely high, in the case of a single dose of Infanrix Hexa vaccine, approximately 8000 times higher than is required to kill a salmon parr within forty-eight hours. Even allowing for some dilution of the injected aluminium adjuvant into body fluids bathing and innervating the tissues surrounding the injection site the total concentration of aluminium in a vaccine is sufficient to cause cell death within hours and perhaps minutes of receiving the injection. This is the definition of an acute response, death (cells or whole organism) within a short period of exposure to a toxin. It is a necrotic form of cell death. It initiates an inflammatory response (redness at the injection site). This inflammation drives and perhaps accelerates the subsequent immune response (here). A number of mechanisms bring about remediation of acute aluminium toxicity at a vaccine injection site. These are chemical, physical and biological. The toxic free metal ion, Al3+, forms soluble and insoluble complexes with myriad biological molecules while particles of aluminium adjuvant and other insoluble aluminium compounds are taken up by cells infiltrating the vaccine injection site. All of these processes act to reduce the acute toxicity of aluminium at the injection site by lowering the immediate concentration of toxic Al3+. These remedial processes act to secure aluminium in a number of different compartments. All are systemic and all are potential sources of biologically reactive aluminium to the rest of the body. Many chemical compartments where aluminium is bound in myriad different complexes including simple organic moieties like citrate or more complex proteins like the iron transport protein transferrin promote the transport of aluminium away from the injection site. These processes can be envisaged as continuous passive diffusion of soluble aluminium away from the injection site. The majority of injected aluminium adjuvant is particulate in the first instance and actively taken up, literally eaten, by a number of different cells infiltrating the injection site. Some particles of aluminium adjuvant are taken up by macrophages and thereafter they are retained at or close to the injection site as a granuloma. Generally, these collections of macrophages are considered as benign ‘cancers’ though such descriptions have been coined for situations where the cellular cargo is not aluminium. For example, macrophagic myofasciitis or MMF is a disease, first described by Romain Gherardi in Paris, in which aluminium-rich granulomas at vaccine injection sites are implicated in disease aetiology. Other cells heavily laden with aluminium do not remain close to the injection site and carry their cargo well beyond where the vaccine is administered, for example visiting local lymph nodes as early stops on their travels. Evidence is mounting that these cells may transport aluminium into brain tissue using both lymph and blood as access routes. Perhaps most worrying, evidence of transport of aluminium into brain tissue across the blood-brain barrier and meninges has been shown in autism (here). Read more and comment at The Hippocratic Post.