An autoimmune disease occurs when the immune system of the body produces antibodies against its own tissues. Research confirms that the root cause of many undesired immune reactions originate in the gastrointestinal tract.(1)​ The human intestinal epithelium, the thin tissue forming the outer layer, is formed by a single layer of epithelial cells. The space between these cells are sealed by tight junctions, which regulate the permeability of the intestinal barrier. In other words, these tight junctions regulate what molecules, in the intestines, are allowed to enter into the bloodstream. These tight junctions are the “gate keepers”.


When the immune system attacks the intestinal barrier the tight junctions become compromised. The tight junctions become inflamed and the junctions become wider allowing macromolecules, considered by the body as foreign invaders, to enter into the bloodstream. The immune system senses these macromolecules and then produces antibodies to them. These macromolecules can land anywhere in the body, resembling the molecular sequence of tissue (molecular mimicry) or binding directly to the tissue, causing the body's immune system to attack the self-tissue antigens.(1) Patients with chronic inflammatory and autoimmune conditions should be checked for the existence of increased gut permeability by measurement of IgA and IgM antibodies against LPS (lipopolysaccharides - bacterial endotoxins) and tight junction proteins.(1) 


One of the biggest culprits leading to compromised tight junctions is gluten, and in particular alpha-gliadin, a glycoprotein in gluten containing foods (wheat, barley, and rye). Alpha-gliadin contains the toxic peptides associated with celiac disease (a chronic autoimmune reaction to alpha-gliadin where antibodies are produced that attack the intestines and other tissues).(2) Detection of antibodies to alpha-gliadin may indicate abnormal mucosal immune response and intestinal barrier dysfunction.  ​Current testing for gluten sensitivity and celiac disease includes serum IgG and IgA antibodies against alpha-gliadin and tissue transglutaminase-2 (an enzyme that is used by the body to form barriers and stable structures).(2) Those individuals with positive serologies should have a tissue biopsy for a diagnosis of celiac disease.(3)


​A negative serology does not necessarily mean a negative immune reaction or negative pathology. Several reports show that the majority of celiac patient's antibodies to alpha-gliadin may be negative.(2) How can this be? The reason for this is that wheat not only contains alpha-gliadin but also additional proteins such as omega-gliadin, glutenin, gluteomorphin, prodynorphin, and agglutinins, all of which can cause an immune system reaction and are not being tested.(2)


A person can have symptoms associated with celiac disease when they eat gluten products, but not have celiac. This is called non-celiac gluten sensitivity or NCGS. Although, as stated below, both NCGS and celiac disease can lead to autoimmune diseases. Common symptoms of a gluten related disorder with or without celiac disease:(3)


  • ​Anemia (iron-deficiency) that does not respond to iron therapy
  • ​Bone density issues such as osteopenia (mild) or osteoporosis (severe)
  • Chronic anxiety or depression
  • Chronic diarrhea or constipation
  • Chronic fatigue
  • Delayed puberty
  • Failure to thrive or short stature
  • Liver and biliary tract disorders
  • Pain in joints
  • Pale, foul-smelling stools
  • Pale sores inside of mouth
  • Peripheral neuropathy
  • Recurring abdominal bloating and pain
  • Skin rash
  • Tingling numbness in the legs
  • Tooth discoloration or loss of enamel
  • Unexplained infertility, recurrent miscarriage
  • Unexplained weight loss
  • Vomiting


Some interesting facts to consider:


  • Antibodies to gluten can circulate in the bloodstream, causing collateral damage and excessive inflammation for as long as 3 to 5 months.(3) Consuming gluten while there are still circulating antibodies is like throwing gasoline onto the fire. With this information, it is easy to understand how eating gluten can delay any recovery for months, keeping the body in a state of chronic degeneration. 


  • An estimated 72 million people in the United States, or approximately 22% of the population, have an autoimmune disease.(3)


  • People with gluten sensitivity (NCGS) develop the same types of symptoms as people with celiac disease when exposed to gluten. If NCGS is left untreated, it will progress to the same degenerative autoimmune diseases as people with celiac disease.(3)


  • ​Gluten sensitivity in and of it's self is a systemic autoimmune disease.(3)


  • No human can completely digest the toxic gluten proteins found in wheat, rye, and barley.(3)


  • Gluten in wheat causes intestinal permeability in every human.(3)


  • The gluten content in grains has increased over the past 50 years due to hydridization. This makes the digestibility of today's grains much more difficult than the grains you have grown up eating.(3)


  • Researchers have found that all humans develop intestinal permeability whenever they're exposed to gluten, regardless of whether or not they have celiac disease or gluten sensitivity.(3)


  • ​Cow's milk plays a role in the gastrointestinal symptoms in 50% of patients with gluten sensitivity and celiac disease.(3)(5)


  • ​Cow's milk may also be one of the causes of multiple sclerosis (MS). Multiple retrospective population based studies in the United States, European countries, Japan, Australia, and South Africa show a correlation between MS with cow's milk consumption. There is a high sequence of similarity between a major protein of milk fat globule membrane called butyrophilin and myelin oligodendrocyte glycoprotein (a glycoprotein that is important in the myelination of nerves). This is an example of how molecular mimicry plays a role in autoimmune diseases.(6) 


  • ​The demonstration of molecular mimicry between alpha-gliadin, cerebellar peptide, milk butyrophilin, and myelin oligodendrocyte glycoprotein may have broader implications in the induction of neuroimmune disorders.(6)


A partial list of some autoimmune disorders, credited by the American Autoimmune Related Diseases Association.(4)


  • Addison's disease
  • Alopecia areata
  • Alzheimer's
  • Amyotrophic lateral sclerosis (ALS), AKA: Lou Gehrig's disease
  • Ankylosing spondylitis
  • Autoimmune aplastic anemia
  • Autoimmune hepatitis
  • Autoimmune hyperlipidemia
  • Autoimmune immunodeficiency
  • Autoimmune myocarditis
  • Autoimmune pancreatitis
  • Autoimmune retinopathy
  • Autoimmune thrombocytopenic purpura (ATP)
  • Autoimmune thyroid disease
  • Behcet's disease
  • Cardiomyopathy
  • Celiac disease
  • Chronic fatigue syndrome
  • Chronic inflammatory demyelinating polyneuropathy
  • Chronic recurrent multifocal osteomyelitis
  • Congenital heart block
  • Crohn's disease
  • Demyelinating neuropathies
  • Dermatitis herpetiformis
  • Dermatomyositis
  • Endometriosis
  • Fibromyalgia
  • Glomerulonephritis
  • Grave's disease
  • Guillain-Barre syndrome
  • Hashimoto's encephalitis
  • Hashimoto's thyroiditis
  • Hemolytic anemia
  • Hypogammaglobulinemia
  • Idiopathic pulmonary fibrosis
  • Idiopathic thrombocytopenic purpura (ITP)
  • IgA nephropathy
  • IgG4-related sclerosing disease
  • Juvenile arthritis
  • Juvenile diabetes type 1
  • Kawasaki disease
  • Lichen planus
  • Lupus (SLE)
  • Lyme disease, chronic
  • Multiple sclerosis (MS)
  • Myasthenia gravis
  • Neutropenia
  • Optic neuritis
  • Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS)
  • Peripheral neuropathy
  • Primary sclerosing cholangitis
  • Psoriasis
  • Psoriatic arthritis
  • Raynaud's phenomenon
  • Reactive arthritis
  • Reflex sympathetic dystrophy
  • Reiter's syndrome
  • Relapsing polychondritis
  • Restless leg syndrome
  • Retroperitoneal fibrosis
  • Rheumatic fever
  • Rheumatoid arthritis
  • Sarcoidosis
  • Scleroderma
  • Sjogern's syndrome
  • Subacute bacterial endocarditis (SBE)
  • Susac's syndrome
  • Temporal arteritis
  • Thrombotic thrombocytopenic purpura (TTP)
  • Type 1 diabetes
  • Ulcerative colitis
  • Uveitis
  • Vasculitis



The protocol, in part, will consist of changing the diet and healing the gut, as one would expect. Abstaining from all gluten containing foods is a priority! We will also test for other food allergies to avoid any further intestinal inflammation and evaluate for heavy metal toxicity. Additionally, we will then recommend specific products to heal the damaged intestinal tissue and restore those tight junctions.

Please contact us for more information.


References:


1) Cyrex Laboratories. 2012. Clinical Application Guide to Intestinal Antigenic Permeability Screen

2) Cyrex Laboratories. 2012. Wheat/Gluten Proteome Reactivity & Autoimmunity

3) O'Bryan, Tom. 2016. The Autoimmune Fix. New York, NY. Rodale Inc. pp. 13, 16, 21, 28, 43, 44, 46, 61

4) AARDA. Retrieved from http://www.aarda.org/autoimmune-information/list-of-diseases/

5) Cyrex Laboratories. 2012 Gluten-Associated Cross-Reactive Foods & Food Sensitivity

6) Cyrex Laboratories. 2012 Multiple Food Immune Reactivity Screen


 

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