Multiple sclerosis (MS) is an inflammatory disease in which the insulation (myelin sheaths) of nerve cells in the brain and/or spinal cord are eroded, disrupting the ability of parts of the nervous system to efficiently transport synaptic information without it leaking. This results in a wide range of chronic physical and mental symptoms that predispose to psychological instability. Deterioration generally occurs as sudden stages with the occurrence of new chronic symptoms, or through continual degeneration which gradually increases the severity of symptoms over time. Sometimes symptoms disappear, however if re-myelination cannot be permanently created, the disease will advance.
While the cause is not yet clear to science, the underlying mechanism is thought to be either inappropriate targeting of the myelin-producing cells by the immune system or failure of the myelin-producing cells to maintain the sheaths. Professor Michael Pender – who is the director of the Multiple Sclerosis Research Centre at the University of Queensland’s School of Medicine, and directs the Multiple Sclerosis Clinic at the Royal Brisbane and Women’s Hospital – has for several years focused research on the Epstein-Barr virus (EBV) as the principal behind MS.
The Epstein–Barr virus is a superantigen virus of the herpes family, and is a principal human virus. It causes glandular fever, and is associated to varying degrees with many cancers and autoimmune diseases including MS. More than 90 per cent of the world’s population permanently has the virus. While most people develop fragile adaptive immunity to this virus, if a person’s adaptive immune system deteriorates in a specific aspect of its communication efficiency, this virus will reactivate and can greatly reduce immune system effectiveness and efficiency by controlling B-cell focus and subverting CD8 T-cells.
Inappropriate B-cell activity has been linked to the damage of nerve fibres that is consistent with that observed in MS. There is a theory that EBV infected B-cells are able to congregate in the brain/spinal cord because cytotoxic CD8 T-cells (the immune system cells that target viral-infected cells, including B-cells) become incapable of identifying strongly infected B-cells—because the active virus re-codes newly created T-cells when they attempt to inspect the infected B-cells for the first time.
Professor Pender and his colleagues have been investigating whether improving CD8 T-cell recognition against these EBV-infected B-cells (immunotherapy) could be used as an effective therapy for MS.
With this new technique, T-cells are extracted from the blood of an individual with secondary progressive MS, and incubated along with fragments of the Epstein-Barr virus. This enables the T-cells to more effectively identify the virus without the concern of being subverted. When the T-cells are injected back into the person, they are able to increase their targeting of EBV infected B-cells. It is highly possible that this type of technique could be used as a therapy to reduce, or even halt, the progression of MS.
For more than 20 years we have been using a similar immunotherapy approach in our clinic. The difference is that we have been using specific homoeopathic nosode combinations (authoimmunosodes) made from the two types of EBV, sometimes in combination with cytomegalovirus and Human herpes-7, to improve CD8 T-cell recognition of infected B-cells. We have recorded good success with this approach, in combination with unloading T-cells activity through molecular mimicry responses between plant defence chemicals and the Epstein-Barr virus. We determine a dose strength and repeat rate specific to an individual to achieve good long-term results.
Over thousands of case studies using authoimmunisations for other types of autoimmune diseases, it had been apparent to us that better CD8 T-cell responses occur when the work load of these cells is reduced and their ability to more clearly communicate with other cells including B-cells, is improved. We achieve this by removing immune contact with specific plant agglutenins, glutelines, albumines, globulines, prolamines and other storage/defence/toxic chemicals (in less than 10 parts per million). We also work to improve an individual’s lymph, liver and kidney function. A necessary part of this approach to heal MS is to address emotional responses to specific personal beliefs as well as provide specific corrective exercises when they start to improve.
It is highly probable that combining the approach of Professor Pender with the lifestyle and homoeopathic immunotherapy approach I have used, could further increase the chances for total remission from MS. For information about EBV and molecular mimicry, contact us for your copy of No More Chronic Fatigue—improving immune strength and efficiency by Bill Giles.