I am not a medical expert. The opinions expressed here are my own personal opinions. Use information on this web site at your own risk.

As a person diagnosed with Multiple Sclerosis (MS), I hope this site will be accepted with the understanding that once auto immune diseases are understood, I will stop breaking my 'butt' on this study...

Later in this page, I have inserted a table of what are considered autoimmune diseases. In the first column is a link to some support structure for the disease including information that someone diagnosed with the disease would like to have.

I have attempted to produce a self consistent theory that might explain MS (and possibly other auto immune diseases).

Introduction

I have had Multiple Sclerosis (MS) since 1977, though I was not diagnosed until 1991. I started as Relapsing/Remitting and became Secondary/Progressive (and retired) at the end of 1997. As I began to read more about MS, on various Forums, I became aware of a surprisingly large number of instances of people with multiple auto immune diseases (I have MS and Pernicious Anemia).
 

Much of the medical community appears to not have a firm understanding of why/how auto immune diseases occur. As I understand it, the antibodies that are the 'memory' of the immune system are checked for 'accuracy' (either the target is 'self' or 'not self') by the thymus; antibodies that attack 'self' are not released. There has been recent research on the immune system that has indicated that immune system B-cells are self propagating and are not reviewed by the thymus.
 

In my reading, I became aware of a possible explanation for auto immune diseases.

Consider, first, that the immune system exists as it does, primarily because of evolution. Therefore, anything that inhibits human reproduction will be selectively removed from the genetic structure. Thus, if any attribute of a disease reduces the likelihood of reproduction (most likely, by or prior to the age of 35-45 years of age), that attribute will be selected against.

I believe that evolution will also have established that if the immune system is involved in/reacting to a disease, it must be responding to 'foreign' material. This means that there must be a pathway for the foreign material to reach the blood system. Obvious pathways are: the air we breath, broken skin barrier (or passage through this barrier) and via the food/liquid that we ingest. The pathway that I suspect is the digestive tract. Normally, in the digestive tract, food plus enzymes and hydrochloric acid pass down the small intestine. When the food has been digested (reduced to amino size portions), it should be absorbed through a semi permeable membrane between the small intestine and the blood stream. If this membrane is hyper permeable, it would permit larger than normal molecules to reach the blood stream, which could produce an immune response because of the 'foreign' material now in the blood system.
 

Hyper permeability in the small intestine (also called Leaky Gut Syndrome  ref, ref, ref, ref, ref, ref) could be the result of inappropriate organisms taking residence in the small intestines. In a healthy individual, the normal organisms (bacteria providing assistance with digestion) are rhamnosus, acidophilus and bifidus (ref?). These bacteria are adapted to the hydrochloric acid present in the digestive tract and help to keep other bacteria from taking residence. Therefore reduced hydrochloric acid production (hypochlorhydria) could result in inappropriate bacteria becoming resident in the small intestine. This may explain why many, if not all, of the list of autoimmune diseases normally having an onset age of 35 or older. Evolution would be unlikely to select against a condition producing a reduction in hydrochloric acid production, if it occurred later in life, than would be 'normal' for human reproduction. This may account for the indication that there is a genetic aspect to susceptibility to autoimmune diseases.
 

However, the literature mentions many instances of autoimmune disease occurring at a much younger age. Antibiotics may be responsible here, as they can readily 'kill off' the normal (good) bacteria in the small intestine, which can lead to the growth and presence of inappropriate bacteria which, can in turn, lead to hyper permeability. Once an immune response has been produced (to a random protein strand), the response will persist because of 'memory' in the immune system; this can include any of the autoimmune responses.

If my theory holds water, two issues need to be dealt with:

• checking the acid level in the stomach and small intestine and correcting it if it is not correct;

• healing the small intestine lining by ensuring that the bacteria in the small intestines are appropriate.

For me, this approach appears to have reduced my exacerbation rate nearly to zero for the last two years. While I still have deficits from my MS, I continue to look for a solution, possibly in the approach mentioned in the B-cell article.

Where to go from here?

I approached this question from the viewpoint of MS, but little that I have mentioned is specific to MS - only to autoimmune diseases. Much of my follow up work will be directed to review of other AI diseases.

AutoImmune Diseases

Disease	Why Considered AI
Alopecia Areata	PubMed Abstract
Ankylosing Spondylitis	BMJ Publishing Group, PubMed Abstract
Antiphospholipid Syndrome
Autism
Autoimmune Addison's Disease
Autoimmune Hemolytic Anemia
Autoimmune Hepatitis
Behcet's Disease
Bullous Pemphigoid
Cardiomyopathy
Celiac Sprue-Dermatitis
Chronic Fatigue Immune Dysfunction Syndrome (CFIDS)
Chronic Inflammatory Demyelinating Polyneuropathy
Churg-Strauss Syndrome
Cicatricial Pemphigoid
CREST Syndrome
Cold Agglutinin Disease
Crohn's Disease
Discoid Lupus
Essential Mixed Cryoglobulinemia
Fibromyalgia-Fibromyositis
Graves' Disease
Guillain-Barre
Hashimoto's Thyroiditis
Idiopathic Pulmonary Fibrosis
Idiopathic Thrombocytopenia Purpura (ITP)
IgA Nephropathy
Insulin dependent Diabetes
Juvenile Arthritis
Lichen Planus
Lupus
Meniere's Disease
Mixed Connective Tissue Disease
Multiple Sclerosis
Myasthenia Gravis
Pemphigus Vulgaris
Pernicious Anemia
Polyarteritis Nodosa
Polychondritis
Polyglandular Syndromes
Polymyalgia Rheumatica
Polymyositis and Dermatomyositis
Primary Agammag-lobulinemia
Primary Biliary Cirrhosis
Psoriasis
Raynaud's Phenomenon
Reiter's Syndrome
Rheumatic Fever
Rheumatoid Arthritis
Sarcoidosis
Scleroderma
Sjogren's Syndrome
Stiff-Man Syndrome
Takayasu Arteritis
Temporal Arteritis/Giant Cell Arteritis
Ulcerative Colitis
Uveitis
Vasculitis
Vitiligo
Wegener's Granulomatosis

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