What is Autoimmune Disease?

Intestinal Health

Usually, autoimmune disease starts with impaired gut permeability caused by various factors including over-exercise, inflammatory foods, stress, and exacerbated by alcohol. The gut accounts for 40% of our total energy expenditure. The gut lining prevents against loss of water and electrolytes and entry of antigens and microorganisms into the body. While allowing the exchange of molecules between host and environment and absorption of nutrients in the diet.

The gut functions as a complex multilayer system (1). The lining comprises an outer physical barrier and an inner functional/immunological barrier. The interaction of these 2 barriers enables permeability to be maintained. Disruption of these barriers results in severe immunodeficiency and risk of disease. Loss of intestinal barrier functions can occur abruptly in response to a major trauma such as severe burns and multi-organ failure. It can also occur gradually, leading to chronic inflammatory diseases.


The gut barrier

The gut lining comprises the endothelium, the epithelial cell lining, and the mucus layer. There are also biochemical substances take part in the barrier function including digestive secretions, immune molecules (i.e. IgA and regulatory T cells), inflammatory mediators and antimicrobial peptides. The intestinal microbiota acts to modulate the gut lining but is often not considered part of the barrier. Once the gut becomes permeable, food particles and various other things pass into general circulation. Under normal circumstance, your digestive system would do its job and digest food and bind environmental contaminants to bile salts for detoxification.


The function of tight junctions

Gut Lining

The epithelial cells lining the gut are sealed by tight junctions and adherence junctions. Tight junctions regulate the flow of water ions and small molecules through the gut lining. Adherence junctions are important in cell-cell signaling and help to maintain epithelial stability. The stability of the tight junction system is regulated by zonulin and zonulin receptors (2). When activated by zonulin the tight junctions separate allowing proteins and bacteria to enter circulation. In a compromised gut, undigested protein, pathogenic bacteria and any accompanying environmental junk can pass through your gut lining into general circulation. Once in circulation, your immune system must process it until it can circulate back to your liver for detoxification.

The problem occurs when rogue contaminants come into contact with various tissues throughout the body. Once in contact with these tissues, the immune system is activated to clear out these contaminants. Eventually, the immune system (T cell antigens) begins to make antibodies that target the tissues the contaminant migrates to. The immune system begins to see your own bodily tissues as an invader.


How is an autimmune disease determined?

The various types of autoimmune diseases depend on which organ system the body identifies as an intruder. This can be different for every individual even if the cause of the autoimmunity is the same. Usually, when the source of the immune reaction is corrected, the organ system that has been affected must also be supported as well. This is what people find confusing because once the offending foods/contaminants are removed and people feel better, they often find that the disease process will persist. There is a difference between stopping damage and repairing the damage.


Let the healing begin

Once the damage has ceased, it can take time to heal and if left for too long, a full recovery may not be possible. The first to step to healing and recovery is removing the agent activating the immune response. Once removed, and the inflammatory response has concluded, the body can repair itself. After the conclusion of the inflammatory response, people often feel significantly better and find that their symptoms improve anywhere from 50 to 70%. Even though they feel better, they are often frustrated that the other 50 to 30% seems to take forever, this is because the actual healing process takes time.

The inflammatory response can conclude rather quickly and create a false expectation for the rest of the healing process which can take years. The stress that this false expectation can further prolong the healing process and may even reactivate the inflammation process. Really, the best medicine is time, consistency and patience. First, the gut needs to heal and once that occurs, the affected organ system can start to heal.


Wait, inflammation can be good?

Another potential issue is that inflammation can be protective, which is why sometimes you hear about people getting worse after they show remarkable improvement. Inflammation can create a barrier that protects us from internal and external damage even though it makes us feel like garbage. Once the inflammation is eliminated, the body attempts to resume normal functioning and can struggle until sufficient healing occurs.


The list of autoimmune related diseases is impressive to say the least and because there can be multiple effects on the same organ system, there is substantial overlap in disease states. There are numerous autoimmune diseases that affect the eyes, skin, nerves, myelin sheath, brain, endocrine organs, and gut. This amount of overlap can make an accurate diagnosis very difficult.


What can you do?

Often, the best thing we can do is find and remove the autoimmune triggers, heal the gut, manage inflammation and support the body’s natural detoxification system. Easier said than done, as anyone suffering with an autoimmune diseasae will tell you. Sometimes an autoimmune trigger can be complicated if it is caused by heavy metal contamination, toxins such as molds and/or other environmental contaminants that can take time to excrete from the body. I usually suggest testing to make sure the correct autoimmune triggers are identified, especially if there isn’t improvement after removing the most common triggers.

Once the body can successfully detox, absorb and distribute nutrients again, the healing process can begin.


Non-comprehensive list autoimmune related diseases:

Addison’s disease

Alopecia areata


Antiphospholipid syndrome

Autoimmune angioedema

Autoimmune dysautonomia

Autoimmune encephalomyelitis

Autoimmune hepatitis

Autoimmune inner ear disease (AIED)

Autoimmune myocarditis

Autoimmune pancreatitis

Autoimmune retinopathy

Autoimmune urticaria

Axonal & neuronal neuropathy (AMAN)

Celiac disease

Chronic inflammatory demyelinating polyneuropathy (CIDP)

Crohn’s disease

Dermatitis herpetiformis


Dressler’s syndrome



Fibrosing alveolitis


Graves’ disease

Hashimoto’s thyroiditis

Hemolytic anemia

Hidradenitis Suppurativa (HS) (Acne Inversa)

IgA Nephropathy

Interstitial cystitis (IC)

Juvenile arthritis

Juvenile diabetes (Type 1 diabetes)

Juvenile myositis (JM)

Ligneous conjunctivitis

Linear IgA disease (LAD)


Lyme disease chronic

Meniere’s disease

Mixed connective tissue disease (MCTD)

Multifocal Motor Neuropathy (MMN) or MMNCB

Multiple sclerosis

Myasthenia gravis



Neuromyelitis optica

Optic neuritis

Palindromic rheumatism (PR)


Peripheral neuropathy

Perivenous encephalomyelitis

Pernicious anemia (PA)

Polyarteritis nodosa

Polymyalgia rheumatica


Postmyocardial infarction syndrome

Postpericardiotomy syndrome

Primary biliary cirrhosis

Primary sclerosing cholangitis

Progesterone dermatitis


Psoriatic arthritis

Pure red cell aplasia (PRCA)

Raynaud’s phenomenon

Reactive Arthritis

Reflex sympathetic dystrophy

Relapsing polychondritis

Retroperitoneal fibrosis

Rheumatoid arthritis



Sjögren’s syndrome

Sympathetic ophthalmia (SO)

Tolosa-Hunt syndrome (THS)

Type 1 diabetes

Ulcerative colitis (UC)



  1. Bischoff, S. C., Barbara, G., Buurman, W., Ockhuizen, T., Schulzke, J. D., Serino, M., … & Wells, J. M. (2014). Intestinal permeability–a new target for disease prevention and therapy. BMC gastroenterology, 14(1), 189.

2. Fasano, A. (2012). Zonulin, regulation of tight junctions, and autoimmune diseases. Annals of the New York Academy of Sciences, 1258(1), 25-33.

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