MIT concepts explains MIASMS in terms of chronic disease dispositions caused by ANTIBODIES or DEFORMED PROTEINS. This explanation helps us to approach those so-called AUTO IMMUNE DISEASES from a new angle.
Let us look into the exhaustive list of diseases included in the class of AUTO-IMMUNE DISEASES, which are actually ‘chronic diseases caused by off-target actions of antibodies’. Kindly go through this list to realize the real magnitude of ‘anti-body’ mediated diseases or ‘miasmatic’ diseases in our day today medical practice:
” Acute disseminated encephalomyelitis, Acute hemorrhagic leukoencephalitis, Addison’s Disease, Agammaglobulinemia, Alopecia areata, Amyotrophic Lateral Sclerosis, Ankylosing Spondylitis, Anti-GBM/TBM Nephritis, Antiphospholipid syndrome, Antisynthetase syndrome, Atopic allergy, Atopic allergy, Atopic dermatitis, Autoimmune aplastic anemia, Autoimmune cardiomyopathy, Autoimmune enteropathy, Autoimmune hemolytic anemia, Autoimmune hepatitis, Autoimmune inner ear disease, Autoimmune lymphoproliferative syndrome, Autoimmune peripheral neuropathy, Autoimmune pancreatitis, Autoimmune polyendocrine syndrome, Autoimmune thrombocytopenic purpura, Autoimmune progesterone dermatitis, Autoimmune urticaria, Autoimmune uveitis, Balo disease/Balo concentric sclerosis, Bechets Syndrome, Berger’s disease, Bickerstaff’s encephalitis, Blau syndrome, Bullous pemphigoid, Cancer, Celiac disease, Castleman’s disease, Chronic inflammatory demyelinating polyneuropathy, Chronic recurrent multifocal osteomyelitis, Churg-Strauss syndrome, Cicatricial pemphigoid, Cogan syndrome, Cold agglutinin disease, Complement component 2 deficiency, Cranial arteritis, CREST syndrome, Crohns Disease, Cushing’s Syndrome, Cutaneous leukocytoclastic angiitis, Dego’s disease, Dercum’s disease, Dermatitis herpetiformis, Dermatomyositis, Diabetes mellitus type 1, Discoid lupus erythematosus, Eczema, Erythema nodosum, Diffuse cutaneous systemic sclerosis, Enthesitis-related arthritis, Epidermolysis bullosa acquisita, Eosinophilic gastroenteritis, Eosinophilic fasciitis, Dressler’s syndrome, Diffuse cutaneous systemic sclerosis, Essential mixed cryoglobulinemia, Evan’s syndrome, Fibrodysplasia ossificans progressive, Fibrosing aveolitis, Gastritis, Gastrointestinal pemphigoid, Giant cell arteritis, Glomerulonephritis, Goodpasture’s syndrome, Graves’ disease, Henoch-Schonlein purpura, Guillain-Barré syndrome, Hashimoto’s encephalitis, Hashimoto’s thyroiditis, Haemolytic anaemia, Herpes gestationis, Hypogammaglobulinemia, Idiopathic Inflammatory Demyelinating Diseases, Idiopathic pulmonary fibrosis, Idiopathic thrombocytopenic purpura, IgA nephropathy, Inclusion body myositis, Inflammatory demyelinating polyneuopathy, Interstitial cystitis, Juvenile idiopathic arthritis, Juvenile rheumatoid arthritis, Kawasaki’s Disease, Lambert-Eaton myasthenic syndrome, Leukocytoclastic vasculitis, Lichen planus, Linear IgA disease, Lichen sclerosus, Lou Gehrig’s disease, Lupoid hepatitis, Lupus erythematosus, Majeed syndrome, Ménière’s disease, Microscopic polyangiitis, Miller-Fisher syndrome, Mixed Connective Tissue Disease, Morphea, Mucha-Habermann disease, Multiple sclerosis, Myasthenia gravis, Myositis, Neuromyelitis optica, Neuromyotonia, Occular cicatricial pemphigoid, Opsoclonus myoclonus syndrome, Ord thyroiditis, Palindromic rheumatism, pediatric autoimmune neuropsychiatric disorders associated with streptococcus, Paraneoplastic cerebellar degeneration, Paroxysmal nocturnal hemoglobinuria, Parry Romberg syndrome, Parsonnage-Turner syndrome, Pars planitis, Pemphigus vulgaris, Pernicious anaemia, Perivenous encephalomyelitis, POEMS syndrome, Polyarteritis nodosa, Rheumatoid fever, Psoriasis, Polymyalgia rheumatica, Polymyositis, Primary biliary cirrhosis, Primary sclerosing cholangitis, Progressive inflammatory neuropathy, Psoriatic arthritis, Pyoderma gangrenosum, Pure red cell aplasia, Rasmussen’s encephalitis, Raynaud phenomenon, Relapsing polychondritis, Reiter’s syndrome, Restless leg syndrome, Retroperitoneal fibrosis, Rheumatoid arthritis, Sarcoidosis, Schmidt syndrome, Schnitzler syndrome, Scleritis, Scleroderma, Sjögren’s syndrome, Spondyloarthropathy, Still’s disease, Undifferentiated spondyloarthropathy, Stiff person syndrome, Subacute bacterial endocarditis, Susac’s syndrome, Sweet’s syndrome, Sydenham chorea, Sympathetic ophthalmia, Takayasu’s arteritis, Temporal arteritis, Tolosa-Hunt syndrome, Transverse myelitis, Ulcerative colitis, Undifferentiated connective tissue disease, Vasculitis, Vitiligo, Wegener’s granulomatosis”
I have been trying to explain concept of ‘miasms’ as ‘chronic disease dispositions’ due to the ‘off-target’ molecular inhibitions caused by ‘antibodies’ formed against ‘infectious agents’ and ‘exogenous’ proteins. As per this view, antibodies are the causative agents of ‘miasms’.MI
All of us know, so-called ‘autoimmune diseases’ are caused by ‘antibodies’. But, those ‘antibodies’ are considered to be formed not against ‘exogenous antigens’, but ‘endogenous or host antigens’. If we explain ‘miasms’ as ‘antibodies’ formed against ‘exogenous’ proteins, should we exclude ‘autoimmune diseases’ from ‘miasms’, since they are considered to be formed against ‘endogenous antigens’, not ‘exogenous proteins’?
Here, we have to undertake a serious study of the phenomena of ‘autoimmunity’ and ‘autoimmune diseases.
According to immunologists, ‘autoimmune diseases’ arise from an overactive immune response of the body against substances and tissues normally present in the body. In other words, the body actually attacks its own cells. The immune system mistakes some part of the body as a pathogen and attacks it. This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture’s disease which may affect the basement membrane in both the lung and the kidney).
Hundreds of chronic systemic diseases are now classified as ‘autoimmune diseases’. This group include Coeliac disease, diabetes mellitus type 1, systemic lupus erythematosus (SLE), Sjögren’s syndrome, Churg-Strauss Syndrome, Hashimoto’s thyroiditis, Graves’ disease, idiopathic thrombocytopenic purpura, rheumatoid arthritis (RA), lupus and allergies. This group is expanding every day.
Autoimmune diseases are broadly divided into systemic and organ-specific or localised autoimmune disorders, depending on the principal clinico-pathologic features of each disease.
Systemic autoimmune diseases- include SLE, Sjögren’s syndrome, scleroderma, rheumatoid arthritis, and dermatomyositis. These conditions tend to be associated with antibodies to antigens which are not tissue specific. Thus although polymyositis is more or less tissue specific in presentation, it may be included in this group because the autoantigens are often ubiquitous t-RNA synthetases.
Local syndromes which affect a specific organ or tissue:
Endocrinologic: Diabetes mellitus type 1, Hashimoto’s thyroiditis, Addison’s diseaseGastrointestinal: Coeliac disease, Crohn’s Disease, Pernicious anaemia
Dermatologic: Pemphigus vulgaris, Vitiligo
Haematologic: Autoimmune haemolytic anaemia, Idiopathic thrombocytopenic purpura
Neurological: Myasthenia gravis
Autoimmunity is defined as “the failure of an organism to recognize its own constituent parts as self, which allows an immune response against its own cells and tissues. Any disease that results from such an aberrant immune response is termed an autoimmune disease”.
This definition does not answer the question we are interested. Are the antibodies ‘formed against’ native targets, or ‘antibodies formed against’ exogenous antigens mistaking native targets as the ‘exogenous antigens’?
Actually, are the antibodies considered to be the causative agents of ‘autoimmune diseases’ really formed against ‘host antigens’? Or, are they ‘antibodies’ formed against ‘exogenous proteins’ attacking ‘off-target’ sites in the organism?
This topic is still a controversial subject in immunology. We should remember that ‘immune’ mechanism is basically a defense mechanism of our organism to identify and destroy ‘exogenous proteins’ which are alien to our genetic blueprint. Several mechanisms are thought to be operative in the pathogenesis of autoimmune diseases, against a backdrop of genetic predisposition and environmental modulation. It is beyond the scope of this article to discuss each of these mechanisms exhaustively, but a summary of some of the important mechanisms suggested by various hypotheses may be examined.
- T-Cell Bypass – A normal immune system requires the activation of B-cells by T-cells before the former can produce antibodies in large quantities. This requirement of a T-cell can be bypassed in rare instances, such as infection by organisms producing super-antigens, which are capable of initiating polyclonal activation of B-cells, or even of T-cells, by directly binding to the β-subunit of T-cell receptors in a non-specific fashion.
- Molecular Mimicry – An exogenous antigen may share structural similarities with certain host antigens; thus, any antibody produced against this antigen (which mimics the self-antigens) can also, in theory, bind to the host antigens, and amplify the immune response. The idea of molecular mimicry arose in the context of Rheumatic Fever, which follows infection with Group A beta-haemolytic streptococci. Although rheumatic fever has been attributed to molecular mimicry for half a century no antigen has been formally identified (if anything too many have been proposed). Moreover, the complex tissue distribution of the disease (heart, joint, skin, basal ganglia) argues against a cardiac specific antigen. It remains entirely possible that the disease is due to e.g. an unusual interaction between immune complexes, complement components and endothelium.
- Idiotype Cross-Reaction – Idiotypes are antigenic epitopes found in the antigen-binding portion (Fab) of the immunoglobulin molecule. Plotz and Oldstone presented evidence that autoimmunity can arise as a result of a cross-reaction between the idiotype on an antiviral antibody and a host cell receptor for the virus in question. In this case, the host-cell receptor is envisioned as an internal image of the virus, and the anti-idiotype antibodies can react with the host cells.
- Epitope spreading or epitope drift – when the immune reaction changes from targeting the primary epitope to also targeting other epitopes. In contrast to molecular mimicry, the other epitopes need not be structurally similar to the primary one.
If we carefully study the above hypotheses proposed by modern immunology, you will find that all these hypotheses indirectly agree with our contention that so called autoimmune diseases are actually caused by ‘off-target’ inhibitions created by ‘antibodies’ formed against ‘exogenous antigens’
A recent observation regarding relationship of autoimmune diseases and infectious diseases is found to be very important from our ‘miasmatic’ angle. Studies revealed strong association of certain microbial organisms with autoimmune diseases. For example, Klebsiella pneumoniae and coxsackievirus B have been strongly correlated with ankylosing spondylitis and diabetes mellitus type 1, respectively. This has been explained by the tendency of the infecting organism to produce ‘super-antigens’ that are capable of polyclonal activation of B-lymphocytes, and production of large amounts of antibodies of varying specificities, some of which may be self-reactive.
This ‘polyclonal’ ‘super-antigen’ theory goes very close to our explanation of ‘miasms’ as antibody-mediated.
There is a recent proposal among immunologist that the spectrum of autoimmunity should be viewed along an “immunological disease continuum,” with classical autoimmune diseases at one extreme and diseases driven by the innate immune system at the other extreme. Within this scheme, the full spectrum of autoimmunity can be included. Many common human autoimmune diseases can be seen to have a substantial innate immune mediated immunopathology using this new scheme.