The association between Autoimmune Thyroid Disease (AITD) and various other autoimmune diseases was first suggested in the early 1960s. Many studies since then have further cemented the knowledge that you don’t get just one autoimmune disease. If you have one, you likely have more. It just hasn’t been diagnosed yet. Your thyroid is diagnosed by your endocrinologist, while your gastrointestinal issues are being treated by your primary physician and your hormonal issues are taken care of by they gynecologist. None of who are aware of the others. They are doing their job of taking care of their assigned body part.
82% of people with Autoimmune Thyroid also have Autoimmune Gastrointestinal Disease (AIGD) and Anemia.
The anemia is ignored because the “Thyroid” is causing the fatigue. Anemia is not just low iron. The increased frequency of chronic anemia in patients with AITD is essentially due to Autoimmune Atrophic Gastritis occurring at the same time. WHY? A healthy stomach lining is necessary for a healthy red blood cell.
Autoimmune atrophic gastritis is characterized by chronic inflammation and eventual destruction of the stomach lining, which causes nutrient deficiencies and worse. Stomach acid produced in the lining sterilizes our food, killing any microbes while breaking down the food in addition to it role in anemia. Antibiotics that we have all used kill the good bacteria. Antacids neutralize stomach acid setting the stage for atrophic gastritis.
Atrophic gastritis is a condition of chronic inflammation and atrophy (tissue destruction) affecting the stomach’s mucosal lining. Over time, atrophic gastritis leads to a loss of the gastric glandular and chief cells, a subsequent breakdown of the mucosal lining, and an eventual replacement of the mucosa by intestinal and fibrous tissue.
Atrophic gastritis has two causes: 1) an autoimmune process targeting parietal cells or intrinsic factor and 2) environmental causes such as persistent infection with Helicobacter pylori bacteria or dietary factors. Recent evidence suggests that Helicobacter pylori can trigger the development of autoimmune atrophic gastritis through a process of molecular mimicry in which the bacterial organisms take on the appearance of stomach lining. They disguise themselves as the lining tricking the immune system into attacking your body. Evil bastards! How dare they?
In autoimmune atrophic gastritis, autoantibodies cause destruction of the stomach lining. The autoimmune response causes an infiltration of white blood cells and the release of chemical cytokines that accelerate the disease process. Ultimately, the autoimmune response impairs the mucosal cells’ ability to produce hydrochloric acid, digestive enzymes such as pepsin, and intrinsic factor, a substance needed for the absorption of vitamin B12.
Deficiencies of intrinsic factor lead to vitamin B12 deficiency and a condition of pernicious anemia. Deficiencies of hydrochloric acid (hypochlorhydria) fail to stimulate the pancreas to release digestive enzymes, which become trapped in the pancreas. The enzymes then begin to digest the pancreas. Food that is not chemically processed for digestion can sit in the stomach for up to 14 hours at 98.6o. It begins to rot providing the perfect food source for bad bacteria. Early in the course of the disease, symptoms rarely occur although mild symptoms of indigestion may be present.
Autoimmune atrophic gastritis typically causes symptoms related to vitamin B12 deficiency, including anemia, gastrointestinal symptoms, and neurologic symptoms including dementia. Megaloblastic anemia may develop, and rarely platelet deficiency (thrombocytopenia) may occur. Symptoms of anemia include weakness, light-headedness, vertigo, tinnitus, palpitations, angina and symptoms of congestive heart failure. Other symptoms include sore tongue, weight loss, irritability, mild jaundice, and heart enlargement.
The frequency of atrophic gastritis is not known because chronic gastritis does not usually cause symptoms. Females are at higher risk for autoimmune atrophic gastritis with three times as many women affected as men. Patients with other autoimmune disorders, especially autoimmune thyroid disorders, are more likely to develop atrophic gastritis. Atrophic gastritis is the most common autoimmune disease to develop in patients with Graves’ disease who have been treated with radioiodine.
The classical paradigm of autoimmune pathogenesis involving a specific genetic makeup and exposure to environmental triggers has been challenged by the addition of a third element: The loss of intestinal barrier function.
This new theory implies that, once the autoimmune process is activated, it is not self-perpetuating; rather it can be modulated or even reversed by preventing the continuous interplay between genes and environment. As tight junction dysfunction allows this interaction, new therapeutic strategies aimed at re-establishing the intestinal barrier function offer innovative, unexplored approaches for the treatment of these devastating diseases.[i]
The primary functions of the gastrointestinal tract have traditionally been perceived to be limited to the digestion and absorption of nutrients and electrolytes, and to water homeostasis. A more attentive analysis of the anatomic and functional arrangement of the gastrointestinal tract, however, suggests that another extremely important function of this organ is its ability to regulate the trafficking of macromolecules between the environment and your body through a barrier mechanism. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the balance between tolerance and immunity to non-self-antigens. When the finely tuned trafficking of macromoleculesis becomes impaired in susceptible individuals, both intestinal and extraintestinal autoimmune disorders can occur.
This new paradigm subverts traditional theories underlying the development of autoimmunity, which are based on molecular mimicry and/or the bystander effect, and suggests that the autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing intestinal barrier function.[ii]
Autoimmune process can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing intestinal barrier function.
Knowing that 82% of people with Autoimmune Thyroid also have Autoimmune Gastrointestinal Disease (AIGD) and Anemia. In addition to research showing that re-establishing the intestinal barrier function is key to stopping or even reversing autoimmune disease. I look at the variables that impact the barrier in addition to the thyroid and develop a treatment plan specific to a person’s needs.
Is your treatment plan focused on only the thyroid? Are you sick and tired of being sick and tired? Contact us today 530.615.4083 www.wellnessalternatives-stl.com
[i] Fasano, A., and Shea-Donohue, T., Mechanisms of Disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Nature Clin Practice, Gastronenterolo & Hepatol, 2005, 2(9):416-422
[ii] Fasano A., Shea-Donohue T. Mechanisms of Disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. NAT CLIN PRAC GAST HEP. 2005;2:416-422