Lyme Disease: Is ozone therapy can help?
Lyme disease is a bacterial infection caused by a spirochete—a corkscrew-shaped bacterium called Borrelia burgdorferi. Primarily transmitted by black-legged ticks. These tiny arachnids are typically found in wooded and grassy areas. The Centers for Disease Control and Prevention estimate that 300,000 people are diagnosed with Lyme disease in the US every year. Many experts believe the true number of cases is much higher.
The symptoms are so myriad that many people who actually have Lyme may be misdiagnosed with other conditions.
Since diagnosing Lyme can be difficult, doctors tend to avoid diagnosing or label as Lyme’s disease without definitive evidence by positive blood test, however many quarters believe blood test is not accurate with high false negative.
Inadequate early treatment can turn into chronic disease for many years.
Patients with Lyme disease are frequently misdiagnosed with chronic fatigue syndrome, fibromyalgia, multiple sclerosis, and various psychiatric illnesses, including depression. Misdiagnosis with these other diseases may delay the correct diagnosis and treatment as the underlying infection progresses unchecked.
If Lyme disease is not diagnosed and treated early, it may become late-stage or chronic. This may also occur when early treatment is inadequate.
An extensive list of symptoms of chronic Lyme disease was developed by Dr. Joseph Burrascano, a pioneer in treating chronic Lyme disease.
Many Lyme symptoms, such as fatigue, cognitive impairment, joint pain, poor sleep, mood problems, muscle pain, and neurological presentations also occur in other diseases. Hence, the symptoms of Lyme disease significantly overlap those of chronic fatigue, fibromyalgia, rheumatoid arthritis, multiple sclerosis, Parkinson’s disease, ALS, depression and Alzheimer’s disease. Many Lyme patients report being misdiagnosed with a different condition before being properly diagnosed with Lyme disease.
Here, we are not to discuss about sign and symptoms of Lyme’s disease but rather one of the complementary treatment that should be helpful. That is ozone therapy, methodology “extra-corporeal blood ozonation and oxygenation, EBOO”
With this method, disposable materials are use and your blood does not pass through the ozone generator machine therefore no contamination what-so-ever from other people.
Do remember that research on the effect of ozone therapy for Lyme’s disease is very limited or unreliable and none consensus on protocol. However many chronic Lyme’s disease sufferers treated with ozone therapy gave positive remarks subjectively. Theoretically ozone therapy useful for all kind of infection directly or indirectly. No resistance of any bacteria, virus or parasite can develop against ozone, they cannot mutate to develop resistance such as resistance to antibiotic.
Ozone is O3, in the form of gas and using semipermeable membrane dialyzer tube, ozone is taken up immediately by red blood cells that passing through and exert direct and indirect effect to any infection. In case of active viral hepatitis B infection with viral load PCR DNA count in hundreds of millions per ml of blood can reduce in few hundreds after series of ozone therapy. The effect is consistently seen or reproducible. Lyme’s disease is not virus in nature but the point here is any infection whether virus or bacteria can be treated with ozone. For chronic Lyme’s disease, we can expect positive result through indirect after effect of ozone as well.
The effect of ozone are activation of cytokines, interleukin-2 and 20 other interleukins by more than four hundreds percent. Each of interleukin exert multicarious influences alone or in combination with other cytokines on diverse cell types including immunocompetent cells in a network manner. Interferon increase by nine hundreds percent, tumour necrosis factors by three hundred percent. The primary intention with ozone therapy is to promote healing of chronic intractable Lyme’s disease. Look at this table for more details :
|IL-1||T cells||-Stimulates the proliferation and growth of granulocyte
and macrophage colonies from bone
marrow progenitor cells
|IL-2||Activated Th1 cells||– Stimulates the proliferation and growth of antigen primed T cells [TH cells and cytotoxic T cells via (CTL)l
– Co-factor for B cell proliferation and differentiation for lg production
– lnduces LAK activity
– Enhances NK cell activity
– Induces tumour infiltrating lymphocyte (TlL) activity
– Stimulates macrophages and monocytes
|IL-3||TH cells, NK cells, and mast cells||– Promotes the proliferation, survival, and differentiation of multipotent haematopoietic progenitor cells to different lineages such as granulocytes, macrophages, eosinophils, megakaryocytes, and erythrcids
– Stimulates growth and histamine secretion of mast cells, and histamine secretion inhibits THl cell development
|IL-4||Activated TH2 cells||– Co-stimulates the activation of antigen primed B cells
– Stimulates the proliferation and differentiation of B cells
– Induces class switch to lgGl and lgE
– Augments MHC class II molecules,
– Fc receptor, lL-4Ra, lL-ZRB expression mostly on resting B cells
– Stimulates the growth of mast cells and histamine secretion
|IL-5||TH2 cells||– Stimulates he proliferation and differentiation of B cells, induces class switch to IgA
– Promotes the growth and differentiation of eosinophils
|IL-6||Monocytes, macrophages, TH2 cells and bone marrow stromal cells||– Promotes the terminal differentiation of B cells into plasma cells
– Stimulates antibody secretion by plasma cells
– Promotes the differentiation of myeloid stem cells
|IL-7||Bone marrow and thymic stromal cells||– Induces the synthesis of hepatic acute-phase proteins
– Induces T cell growth and differentiation
– Enhances neuronal survival
– Induces thymocyte growth
– Induces T cell growth
– Induces pre B-cell growth in mice but not in humans
– Augments expression of IL-2 and its receptor
|IL-8||Macrophages and endothelial cells||– Contributes to chronic and acute inflammatory reactions
– Chemotactic for neutrophils and T cells
|IL-9||Activated Th2 cells||– Induces growth of TH cells
– In mouse, stimulates erythyroid progenitors, B cells, mast cells, and foetal thymocytes
|IL-10||Activated TH2 cells, B cells, monocytes and keratinocytes||– Suppresses cytokine (IL-2, IL-3, IF N-y, GM-CSF, and TNF) production and thus inhibits cytokine production by TH1 cells
– Down regulates MHC class II expression
|IL-11||Bone marrow stromal cells||– Stimulates the proliferation of lymphoid and haemotopietic progenitor cells
– Promotes the differentiation of B cells
– Promotes the differentiation of megakaryocytes
– Induces the synthesis of acute-phase proteins from hepatocytes
– Induces cardiac hyperthrophy
– Induces osteoclast formation
– Supports the growth of plasmacytomas
|IL-12||Macrophages. B cells and neutrophils||– Promotes the growth of activated T and NK cells and the production of IFN-y by them
– Induces TH1 cell differentiation
– Differentiation of CTL
– Production of IL-2, IL-3, IL-9, GM-CSF and TNF-
|IL-13||Th2 cells||– Inhibits the activation of macrophages and the release of inflammatory cytokines from them|
|IL-15||Monocytes and other cells outside the immune system||– Promotes mast cell growth
– Stimulates NK cell development and differentiation
– Promotes T cell proliferation
|IL-16(proinflammatory)||Peripheral blood mononuclear cells CD4 T cells, mastcells and eosinophils||– Chemoattractant for CD4 T cells, eosinophils and monocytes
– Promots the expression of IL-2R(CD25), HLA-DR as well as the synthesis of IL-3, GM-CSF and IFN-y
|IL-17(pro-inflammatory)||Activated T cells (memory CD4 T cells)||– Induces epithelial and endothelial cells and fibroblasts to produce IL-6, IL-8, G-CSF and PGE2 (haemotopoietic cytokines)|
|IL-18||–||– Augments NK cell activity
– Stimulates human T cells to secrete a large amount of IFN-y )in the presence of IL-12, which induces the expression of the IL-18 receptor on T cells)
|Interferon alpha||Leukocytes||– Inhibits viral replication (including HIV) in different cell types
– Stimulates cytolytic activity in T cells, NK cells, and macrophages
– Effective against certain tumours
|IFN-||Fibroblasts||– Inhibits viral replication
– Stimulates cytolytic activity in T cells, NK cells and macrophages
|IFN-y||TH1, CD8 CTL, and NK cells||– Inhibits viral replication in different cell types
– Enhances the activity of macrophages
– Inhibits the proliferation of TH2 cells
– Increases the expression of MHC class I and class II molecules on many cell types
– Induces class switch to IgG2a; blocks IL-4 induced class switch to IgE and IgGI proliferating B cells
|Ciliary neutrophic factor (CNTF)||Leukocytes||– Enhances the survival of neurons
– Maintains erythroid stem cell pluripotency
– Induces hepatic acute-phase proteins
|Cardiotropin 1 (CT-1)||Leukocytes||– Affects cardiac muscle cells; induce cardiac hyperthrophy
– Maintains erythroid stem cell pluripotency
– Enhances neuronal survival
– Induces hepatic acute-phase protein
|Tumour necrosis factor (TNF)(proinflammatory)||Mainly macrophages; other cell types; NK cells, B and T cells, mast cells, neutrophils, smooth muscle cell||– Cytotoxic to some tumour cells
– Resists intracellular pathogens
– Key regulator
|Lymphotoxin-alpha (LT-)(proinflammatory)||TH1 cells and CTL, B cells||– Cytotoxic and other effects similar to TNF
– Promotes lymph node development