Thyroid disease is an epidemic affecting up to 20 percent of American women. The most common cause of low thyroid today is an autoimmune condition called Hashimoto's Thyroiditis. Like all autoimmune disease, the main feature is the production of antibodies that attack the healthy tissue of the body. In this case, thyroid peroxidase antibodies (TPOAb) and or thyroglobulin antibodies (TgAb) are created against the thyroid.
The roller coaster called Hashimoto's -- it's not a fun ride.
Antibodies wage war against the thyroid, damaging follicles and spilling large amounts of hormone into the bloodstream. Patients experience symptoms of hyperthyroidism or too much thyroid hormone like sudden weight loss, rapid heartbeat, anxiety, high blood pressure and hot flashes. As levels of hormone clear from the blood and drop, patients experience low thyroid symptoms like fatigue, depression, weight gain, constipation and mood swings! This pattern repeats until thyroid hormone becomes depleted. Patients are often diagnosed in a low thyroid state.
How does it develop?
1) It's in the genes. Certain genes in the body increase the chances of becoming autoimmune.
2) Triggers like poor diet, stress, toxins and illness can create negative changes in the microbiome. Friendly bacteria that normally support health become suppressed while opportunistic and pathogenic bacteria take center stage. This can lead to a whole host of health conditions including autoimmunity.
Chemicals and toxins can bind to body cells triggering the creation of antibodies. The immune system will attack the toxin and the cell it's attached to.
Mistaken identity -- The bacteria Yersinia Enterocolitica has been shown to provoke autoimmune attacks through a case of mistaken identity. This bacterium has surface peptides that look like receptors on the thyroid. They are similar enough that when the immune system goes after the Yersinia, it attacks thyroid tissue as well. (1)
Viruses like HTLV-1, enterovirus, rubella, mumps virus, HSV, EBV and parvovirus are all found to be linked with Hashimoto's thyroiditis. These pathogens promote inflammation, provoke overstimulation of the immune system and may create the same type of molecular mimicry seen with Yersinia. Research is still working on finding the exact mechanisms that trigger the self-immune attack in the presence of these viruses. (2)
Hydrogen peroxide is created in the thyroid to help convert iodine to it's usable form. This can be inflammatory without adequate selenium levels to protect tissue by neutralizing free radicals. Selenium deficiency will increase cellular damage and set off autoimmunity. This is one of the reasons the thyroid is so susceptible to the development of Hashimoto's.
Excessive iodine intake can fuel autoimmunity by causing even more hydrogen peroxide to be made. While deficiency can lead to goiter and low thyroid function, too much can make autoimmunity worse.
3) Leaky gut -- the last straw! Tight junctions are like gates between intestine cells forming a protective barrier. Vital nutrients pass through while toxins and pathogens are kept out. Zonulin is a regulatory protein that triggers the temporary opening of these "gates" allowing certain molecules to pass. Gluten is a major trigger for Zonulin over-activity. So are conditions like parasites, candida and SIBO. Similarly, infections, toxins, stress and even a lack of vitamin D can all cause these tight junctions to become weakened and break apart. When the gates are left open large food molecules, pathogens and foreign particles pass into the body setting off a full-scale immune attack. Food intolerances are born, allergies, more inflammation and if you are predisposed-autoimmunity can ensue. (3)
Gluten and antibodies.
There is a clear link between gluten consumption and Hashimoto's Thyroiditis. According to research, the structure of gliadin, a component of gluten, is very similar to thyroid cells. As leaky gut persists and the immune system tags gluten molecules for destruction, thyroid cells get destroyed too. The more gluten you eat, the more antibodies you will make and the more the thyroid will be attacked!
Patients arriving at my office often fall into one of these categories.
1) The patient has been told they have thyroid antibodies but wasn't treated. Instead doctors advised to "watch" it allowing antibodies to run rampant.
2) The patient has symptoms suggesting Hashimoto's but was never tested for antibodies.
3) The patient knows she has Hashimoto's and was treated with thyroid hormone, but the antibodies and underlying condition was never addressed.
All of these scenarios fail the patient.
Antibodies are a sign of some over-activity or misfiring of the immune system that needs to be quieted. Allowing it to persist will only lead to more autoimmunity and more tissue destruction.
Physicians generally order a very limited thyroid blood panel excluding antibodies-mainly because they believe they are untreatable. This is false-we see them normalize all the time.
The standard of care suggests treating patients with replacement thyroid hormone only if the TSH or T4 level is low. I see patients with antibodies and normal hormone levels respond quite well with some form of thyroid medication. Often there is a reduction of symptoms as systems begin to regulate. This is only part of the equation however. Hashimoto's is not a thyroid disease. It is an autoimmune disease that affects the thyroid. This is a very important distinction and one that must be made to fully understand the mechanisms at work and the underlying causes to successfully treat and reverse the condition.
Treatment strategies to tame the autoimmune response.
It's essential to work with a doctor who understands the underlying causes.
Starting with a comprehensive blood panel is the first key element. Levels of TSH, free T3 and T4, total T3 and T4, RT3 and TPO and Tg antibodies must be measured. I also run a specialized test called the TRH stimulation test which allows me to cast a wider net. Even if the regular thyroid panel comes up normal, the TRH will often pick up on missed cases of hypothyroidism (4).
In treating Hashimoto's I begin with healing the gut through the 4R approach. First remove anything that is negatively affecting intestinal health like gluten and other inflammatory foods, toxins, medications, infections, parasites, virus and bacterial overgrowth. Next replace hydrochloric acid and digestive enzymes to aid digestion. Reinocculating the gut with healthy organisms can help regulate the immune system, and fortify the gut wall. Finally glutamine, DGL, aloe and zinc are key ingredients to repair, heal and energize the cells of the intestine.
Vitamin D is very tied to immunity and has been shown to fortify the intestine wall by strengthening tight junctions (5). Further studies find adequate D levels increase cathelicidin antimicrobial peptide or CAMP which is an antimicrobial and antibiotic we make internally (6)! Currently a blood level between 30-100 is considered to be in a healthy range. I find the higher end of the lab range is needed to support proper health. Many patients with antibodies come in with grossly low levels.
Selenium deficiency often plays a roll in autoimmunity. Supplementing with 200-400mcg per day has been shown to reduce thyroid antibodies.
Glutathione is the major antioxidant in the body and can help to further neutralize inflammation and free radicals.
Specialized treatments like UV blood irradiation can oxygenate blood, reset the immune system and kill off harmful bacteria, fungus and viruses that could have been part of the initial immune reaction. Transfer factors are another way to modulate the immune system by boosting the part that is deficient and quieting the part that may be over stimulated.
References:
1) Petru G, et al Antibodies to Yersinia enterocolitica in immunogenic thyroid diseases, Acta Med Austriaca. 1987;14(1):11-4.
2) Rachel Desailloud, and Didier Hober, Viruses and thyroiditis: an update Virology Journal. 2009; 6: 5
3) Alessio Fasano and Terez Shea-Donohue, Mechanisms of Disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases, Nature Clinical Practice Gastroenterology & Hepatology (2005) 2, 416-422
4) Suhail A.R. Doi, et al, TRH Stimulation When Basal TSH is Within the Normal Range: Is There "Sub-Biochemical" Hypothyroidism? Clin Med Res. 2007 Oct; 5(3): 145-148.
5) Kong J, et al, Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. American Journal of Physiology Gastrointest and Liver Physiology. 2008 Jan;294(1):G208-16.
6) Gombart AF, The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Future Microbiology 2009 Nov;4(9):1151-65