, , , ‘Deformed Proteins’ Identified As Causative Factors Of ‘Chronic Diseases’- Theory Of Miasms Ratified! | HOMEOTODAY

MODERN SCIENCE is advancing towards the realization about the TOXIC nature of DEFORMED PROTEINS and their role as a major class of pathogenic agents that cause most of the chronic diseases.
These diseases include AUTO-IMMUNE DISEASES (Acute disseminated encephalomyelitis , Addison’s disease, Agammaglobulinemia, Alopecia areata, Amyotrophic Lateral Sclerosis, Ankylosing Spondylitis, Antiphospholipid syndrome, Antisynthetase syndrome, Atopic allergy, Atopic dermatitis, Autoimmune aplastic anemia, Autoimmune cardiomyopathy, Autoimmune enteropathy, Autoimmune hemolytic anemia, Autoimmune hepatitis, Autoimmune inner ear disease ,    Autoimmune lymphoproliferative syndrome,   Autoimmune pancreatitis,     Autoimmune polyendocrine syndrome , Autoimmune progesterone dermatitis ,   Autoimmune thrombocytopenic purpura,  Autoimmune urticaria,    Autoimmune uveitis, Balo disease/Balo concentric sclerosis,   Behçet’s disease, Berger’s disease,   Bickerstaff’s encephalitis ,  Blau syndrome,   Bullous pemphigoid,   Cancer ,   Castleman’s disease ,  Celiac disease,  Chagas disease,  Chronic inflammatory demyelinating polyneuropathy , Chronic recurrent multifocal osteomyelitis ,  Chronic obstructive pulmonary disease,  Churg-Strauss syndrome,   Cicatricial pemphigoid,  Cogan syndrome,  Cold agglutinin disease,  Complement component 2 deficiency,  Contact dermatitis,  Cranial arteritis,  CREST syndrome,  Crohn’s disease,  Cushing’s Syndrome,  Cutaneous leukocytoclastic angiitis ,   Dercum’s disease,  Dermatitis herpetiformis ,  Dermatomyositis ,  Diabetes mellitus type 1 ,  Diffuse cutaneous systemic sclerosis ,  Dressler’s syndrome ,  Eczema,  Endometriosis ,  Enthesitis-related arthritis,  Eosinophilic fasciitis,   Eosinophilic gastroenteritis , Epidermolysis bullosa acquisita, Erythema nodosum,  Erythroblastosis fetalis ,  Essential mixed cryoglobulinemia, Evan’s syndrome, Fibrodysplasia ossificans progressiva , Fibrosing alveolitis, Gastritis , Glomerulonephritis , Goodpasture’s syndrome, ,Graves’ disease,  Guillain-Barré syndrome, Hashimoto’s encephalopathy, Hashimoto’s thyroiditis, Henoch-Schonlein purpura, Herpes gestationis aka Gestational Pemphigoid, Hidradenitis suppurativa,  Hughes-Stovin syndrome ,
Hypogammaglobulinemia , Idiopathic inflammatory demyelinating diseases, Idiopathic pulmonary fibrosis ,  Idiopathic thrombocytopenic purpura, Inclusion body myositis, Interstitial cystitis, Juvenile idiopathic arthritis, Kawasaki’s disease, Lambert-Eaton myasthenic syndrome, Leukocytoclastic vasculitis ,  Lichen planus,  Lichen sclerosus ,  Linear IgA disease,  Lou Gehrig’s disease, Lupoid hepatitis aka Autoimmune hepatitis, Lupus erythematosus,  Ménière’s disease, Microscopic polyangiitis , Miller-Fisher syndrome, Mixed connective tissue disease, Morphea , Mucha-Habermann disease, Multiple sclerosis, Myasthenia gravis, Myositis , Narcolepsy,  Neuromyelitis optica ,  Neuromyotonia , Occular cicatricial pemphigoid , Opsoclonus myoclonus syndrome , Ord’s thyroiditis, Palindromic rheumatism, PANDAS, Paraneoplastic cerebellar degeneration , Paroxysmal nocturnal hemoglobinuria, Parry Romberg syndrome , Parsonage-Turner syndrome ,  Pars planitis ,  Pemphigus vulgaris ,  Pernicious anaemia ,  Perivenous encephalomyelitis ,  POEMS syndrome , Polyarteritis nodosa ,  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, Rheumatic fever,  Sarcoidosis, Schizophrenia, Schmidt syndrome, Schnitzler syndrome, Scleritis ,  Scleroderma,  Serum Sickness,  Sjögren’s syndrome,  Spondyloarthropathy ,  Stiff person syndrome, Subacute bacterial endocarditis,  Susac’s syndrome ,  Sweet’s syndrome ,  Sydenham chorea,  Sympathetic ophthalmia, Takayasu’s arteritis , Temporal arteritis, Thrombocytopenia, Tolosa-Hunt syndrome,  Transverse myelitis, Ulcerative colitis, Undifferentiated connective tissue disease, Undifferentiated spondyloarthropathy ,  Urticarial vasculitis , Vasculitis, Vitiligo, Wegener’s granulomatosis Etc Etc), AMYLOID DISEASES, PARKINSONS DISEASE, ALZHEIMERS DISEASES, PRION DISEASES, PROTEINOPATHIES, TYPE2 DIABETES, Cerebral β-amyloid angiopathy, Retinal ganglion cell degeneration in glaucoma, Tauopathies , Frontotemporal lobar degeneration , Amyotrophic lateral sclerosis , Huntington’s disease , dementia, Alexander disease, amyloidotic neuropathy, Senile systemic amyloidosis, primary systemic amyloidosis, Aortic medial amyloidosis, Lysozyme amyloidosis, Fibrinogen amyloidosis, Dialysis amyloidosis, Inclusion body myositis/myopathy, Retinitis pigmentosa , Medullary thyroid carcinoma, Cardiac atrial amyloidosis, Pituitary prolactinoma, lattice corneal dystrophy, Cutaneous lichen amyloidosis, Mallory bodies, Corneal lactoferrin amyloidosis, Pulmonary alveolar proteinosis, Odontogenic (Pindborg) tumor amyloid, Seminal vesicle amyloid, Cystic Fibrosis, Sickle cell disease etc etc. This list is growing day by day.
Peculiar three-dimensional conformations resulting from characteristic tertiary folding decides the specific biological roles of protein molecules. If this three-dimensional shape is ‘deformed’ by any way, a protein molecule becomes incapacitated to perform its biological function, and may turn into pathogenic agents.

Proteins could be deformed by various ways:
1. Genetic errors: Presence of faulty genes with wrong nucleotide sequences may result in production of deformed protein molecules.
2. Genetic expression errors: Genetic expression or synthesizing of protein molecules utilizing the genetic blueprints involve a series of systematic biochemical processes involving diverse types of enzymes. Any errors in these enzyme systems may result in the production of deformed proteins
3. Post translational Misfolding : Peculiar three dimensional structures of individual protein molecules synthesized by genetic expression are attained through their post-translational tertiary folding. Errors in mediator enzymes as well as inappropriate intracellular physical environment may result in misfolding of protein molecules.
4. Off-target binding of hormones, enzymes and other endogenous biological molecules: Even though hormones and enzymes have specifically determined roles in biochemical processes, and they are expected to bind only to specific molecular targets for executing these functions, there are occasions when some of them bind to unexpected off-target protein molecules, there by changing their tertiary structures. In such cases, protein molecules get deformed, and may become pathological.
5. Binding with harmful endogenous byproducts such as reactive oxygen species: As part of normal biochemical processes, various harmful reactive molecules such as superoxides are produced in the system, which get instantly destroyed or eliminated by a special defense mechanism working in our body. But in some cases, these hyper-reactive superoxides may bind to essential protein molecules and deform them. Such deformations lead to pathological conditions.
6. Binding with metal ions, toxic drugs or other exogenous molecules.
7. Denaturation by chemicals, ionizing radiations, pH variations, dehydration, abnormal temperature etc.
8. Molecular imprinting by alien proteins such as infectious agents: ANTIBODIES generated against various infectious agents belongs to this class of DEFORMED PROTEINS.
9. Molecular misfolding induced by other deformed proteins: DEFOEMED PROTEINS can act as templates to induce similar proteins also to undergo deformation through a process of molecular imprinting. Prion diseases are found to advance by this process.
It is obvious that DEFORMED proteins cannot perform their SPECIFIC biological functions, which by itself results in pathological conditions.
Moreover, DEFORMED PROTENS can act as PATHOLOGICAL factors in TWO ways.
Deformed proteins bind to totally unexpected biological targets and produce pathological molecular errors. Diverse types of auto-immune diseases and antibody-mediated diseases belong to this class of CHRONIC DISEASES.
Deformed proteins can INDUCE other proteins into MISFOLDING, through a process of MOLECULAR IMPRINTING. Alshiemer’s, Parkinson’s. Prion diseases and various other Amyloid diseases belong to this class.
Various ANTIBODIES generated in the body against  infectious agents and other alien proteins can remain in the body for long periods, and probably induce misfolding in diverse types of native proteins through molecular imprinting. By this way, antibodies act as a major class of pathological factors that cause diverse kinds of CHRONIC DISEASES.
Hahnemann explained CHRONIC DISEASES in terms of MIASMS, which he considered to be the life long disease dispositions caused by INFECTIOUS DISEASES such as itch and leprosy, sexually transmitted genital pappiloma disease, and syphilis. He named these three miasms as PSORA, SYCOSIS and SYPHILIS respectively, of which prime importance was given to PSORA.
Due to limitations of scientific knowledge available during his period, hahnemann could not explain the molecular mechanism by which infectious diseases can produce diverse types of life long chronic diseases. As such, he tried to explain this phenomenon in terms of ‘vital force’ concepts.
With great scientific advancements that happened during last 250 years after hahnemann, we are now in a position to explain how infectious diseases can produce chronic diseases. We know, ANTIBODIES are produced in the body when it get infected. Though antibodies are normally considered to be defense molecules that fight infections, they remain in the body for long periods after infections are over. Since ANTIBODIES are actually globular proteins getting molecular imprinted by ALIEN PROTEINS of infectious gents, these antbodies can act as DEFORMED PROTEINS. Similar to other deformed proteins, ANTIBODIES can act as pathogenic agents by attacking other native proteins, and inducing them to DEFORM.
It is these ANTIBODIES or DEFORMED PROTEINS generated against infectious agents and ALIEN PROTEINS that cause the whole range of CHRONIC DISEASES hahnemann called as MIASMATIC DISEASES.
ANTIBODIES may be playing a causative role in the development of so called AUTO IMMUNE DISEASES, AMYLOID DISEASES and PRION DISEASES by INDUCING deformation in various kinds of native proteins. I hope this possibility also will be considered by the scientists in future. If this prediction is proved to be true, It will be a great recognition of hahnemann’s concept of MIASMS as causative factors of chronic diseases.
Treating DISEASE DISPOSITIONS caused by DEFORMED PROTEINS is a very difficult task even for MODERN MEDICINE. These protein molecules  do not undergo normal biological degrading or destruction. Chemical drugs are no effective in most of such diseases.

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