Hashimoto’s Autoimmune Thyroiditis (Hashimoto’s) is the most common autoimmune disease in the United States, affecting 6-8% of the population, mostly women, who are affected 4-10 times as often as men. Hashimoto’s is an autoimmune disease that affects the thyroid and other tissues. There has been a huge increase in the frequency of Hashimoto’s in recent years, along with large increases in the rates of other autoimmune conditions.
Please note that Hashimoto’s is NOT a thyroid disease; it is an autoimmune disease that affects the thyroid. Unfortunately this distinction seems unimportant to the vast majority of doctors. It is however critical to appropriate treatment by a physician trained in Functional Nutrition. Treating the symptoms of Hashimoto’s does not address the underlying causes of the disease. The standard treatment is simply to prescribe replacement T4 when TSH levels are high, totally ignoring the underlying autoimmune disorder. This treatment is doomed to fail in the majority of cases as it does not consider the root causes that led to the symptoms.
Hashimoto’s was the first recognized autoimmune disorder, described in 1912 by Hakaru Hashimoto. An autoimmune disease is one in which the body’s immune system erroneously recognizes self-tissues as foreign. As a result it mounts an immune response, including the production of antibodies, to destroy what it perceives as a foreign invader. Other examples of autoimmune conditions include rheumatoid arthritis, lupus, and psoriasis. There are currently over 80 identified autoimmune disorders affecting over 50 million Americans.
People with Hashimoto’s have a much higher probability of also having pernicious anemia (antibodies against Intrinsic Factor) and celiac disease (Transglutaminase and Endomysial antibodies), as well as gluten intolerance. There is a 50% probability of developing a second autoimmune disease within 5 years of diagnosis of Hashimoto’s. Neurological disorders due to antibodies directed against the cerebellum and GAD-65 antibodies leading to destruction of pancreatic islet cells and inability to produce the calming neurotransmitter GABA can all occur together.
Hashimoto’s often goes undiagnosed for many years as most physicians only perform TSH levels to evaluate thyroid function, which does not identify the disease. Elevated levels of antibodies directed against the enzyme thyroid peroxidase (anti- TPO Ab) and/or against thyroglobulin (Anti-Tg Ab) are used to diagnose the condition. Diagnostic ultrasound can discern the few cases where antibodies aren’t identified. These tests are included in standard panels offered by Functional Nutrition physicians. In addition to production of antibodies, the immune system mounts a cell-mediated response, infiltrating the thyroid with macrophages, a type of white blood cell, in response to signals from other types of white blood cells called CD-4 and CD-8 helper and cytotoxic T cells. These cells produce, among other things, cytokines, which cause an inflammatory response and cause death of thyroid cells, called apoptosis.
Initially, Hashimoto’s may appear as hyperthyroidism, (Hashimoto’s Thyroiditis) as the production of antibodies causes an increased release of thyroid hormones due to cell damage. It is critical to correctly distinguish this from Grave’s Disease, especially if your doctor is recommending irradiating or removing your thyroid.
Most of the time, there is a slow, gradual progression of the condition due to ongoing attack by autoantibodies. The thyroid becomes enlarged due to progressive damage to thyroid hormone producing cells. The gland develops nodules and irregular diffuse inflammation, with damage and death of the follicles that contain thyroid hormone. Eventually this leads to signs and symptoms of hypothyroidism, which due to their multitude and non-specific nature are often misdiagnosed as depression or other mood or mental disorder, menstrual disorder, chronic fatigue syndrome or fibromyalgia. Often the doctor will treat these symptoms with medications, totally failing to address the underlying condition. Unfortunately, TSH is commonly the only thyroid-related test performed. Unfortunately TSH may not elevate until later in the process, or may not elevate at all for a number of reasons. (See The Trouble with TSH). If you are taking replacement thyroid and continue to need higher doses, it is probable that your thyroid is undergoing progressive destruction from Hashimoto’s.
There are many underlying causes of autoimmunity, including: genetic susceptibility, environmental factors, stress, exposure to toxins, endocrine imbalance, food allergies, Vitamin D deficiency, polycystic ovarian syndrome (PCOS), insulin surges and resistance, gluten intolerance, and Leaky Gut Syndrome.
Women with PCOS have insulin resistance. This causes an increase in the enzyme 17,20 lyase, with increased production of both estrogen and testosterone in the ovaries. The increased testosterone then causes receptor site resistance to insulin, creating a vicious cycle of increasing insulin resistance. Insulin surges cause a shift in the balance of the immune system, which leads to increased cytokine production from the TH-1, or cellular immune system. People with Hashimoto’s tend to have an overactive TH-1 immune system.
Vitamin D deficiency may promote autoimmune conditions, including Hashimoto’s by suppressing what are called T-Reg (Regulatory T cells), which help keep the two parts of the immune system (TH-1 and TH-2) in balance. Some people have a deficiency in the Vitamin D receptor, which makes them more susceptible to a Vitamin D deficiency. Vitamin D is found in high levels in certain lymphocytes and the thymus, the master immune gland. Vitamin D stimulates cytokines that suppresses inflammatory T-cell activity.
Gluten intolerance or sensitivity (which is different than celiac disease) is implicated in numerous health issues, including autoimmune disease. Hashimoto’s patients are much more likely to be gluten sensitive. In my experience 100% of the Hashimoto’s patients I have seen are gluten sensitive. The rate of celiac disease is 200-500% higher in patients with Hashimoto’s than in the non-Hashimoto’s population. Gluten and gliadin are “molecular mimics”. This means that their proteins and protein breakdown products (called polypeptides) look similar to many different tissues in the body as they have amino acid sequences in common. Because of this, when the body is sensitive to gluten and gliadin, it produces antibodies directed against these polypeptides. The antibodies can cross-react to varying degrees with different tissues in the body. Common tissue types that they cross react with include: thyroid, pancreas, nerve (brain, cerebellum), and GI, although there are many other tissue reactions possible. This cross-reaction forms the basis for gluten-mediated autoimmunity.
Warning: Gluten sensitivity is not the same as celiac disease. Do not think that because you have been told that you do not have celiac disease that you are not gluten sensitive. The best way to determine if you are sensitive is to go on a total gluten-free diet, such as the Paleo diet. You must be as close to 100% gluten-free as possible as even a very small quantity will elicit and perpetuate an immune response. If you want laboratory proof that you are sensitive, the gold-standard lab test is the Cyrex Wheat/Gluten proteome Reactivity and Autoimmunity panel.
The vast majority of people with Hashimoto’s are female. Obviously females differ from males genetically, so genetics plays a role in development of Hashimoto’s. Since over 90% of women do not have Hashimoto’s, genetics is not the only factor involved. There are two times in a woman’s life that they tend to develop Hashimoto’s; after pregnancy and around the time of menopause. Both of these times are characterized by major fluctuations of estrogen, which can potentially alter the balance of the immune system.
Toxins are another potential trigger. Many synthetic organic compounds are phytoestrogens, chemicals that can mimic estrogen, which may act as a trigger for autoimmunity.
There are over 50 million compounds that have been isolated from nature or created. The rate of finding new chemicals is increasing exponentially. The majority of people think of toxins as being dose-dependent, in that “the dose makes the toxin”. In other words, we have been taught to believe that low levels do not cause a problem. It is only when a threshold is reached that there is an issue. Unfortunately, this is totally incorrect, for three reasons. Potential toxins (drugs and pesticides for example) are tested individually and their toxicity is rated, based only on the level that causes symptoms. Nothing exists in isolation. No new chemical or drug is tested in combination with others. The potential for interactions is endless, so there is really no accurate way to predict how a toxin will affect an individual.
The second reason this is incorrect is that the major organs of detoxification are the liver and gallbladder. Each individual has a different capacity to detoxify based upon genetics, health of liver and gallbladder and one’s nutritional status, as many essential nutrients are necessary for the detoxification process to function.
Finally, one must consider that many types of toxins can actually bind to various tissues in the body. Separately, neither the toxin (called a hapten), nor the tissue elicits an immune response, however when the two are combined, a new antigen is created. This now creates an immune response that is independent of the dose of the toxin. Mercury is a prime example of this type of reaction. Whereas mercury is highly toxic to the thyroid by itself; the small amount of mercury leached from dental amalgam fillings can cause or contribute significantly to anti-TPO and anti-TG antibody levels. When the fillings were removed, people with Hashimoto’s who also tested positive for mercury sensitivity experienced a significant reduction in autoantibody levels.
In recent years, increased GI permeability or Leaky Gut Syndrome, has been linked to autoimmunity. The GI barrier separates the contents of your intestines, from you. There is only one layer of GI epithelial cells protecting you. These cells are created, do their job, and die in just a few days. They are among the most rapidly dividing cells in the body and therefore require an optimal environment to function properly. Many factors can disrupt this delicate imbalance such as: poor diet with high sugar intake, toxins, chronic use of proton pump inhibitors, antibiotic use which changes the GI microflora, nutritional deficiencies, stress, hormone imbalance, and immune dysfunction.
Normally you are protected against toxins and potential antigens entering your bloodstream by what are called tight junctions between each of the GI epithelial cells, which prevent their free passage, while selectively allowing carbohydrates, fats, amino acids and essential nutrients to enter. When this system starts to break down, partially digested protein can enter your body. This can elicit an immune response, as the body recognizes this as a foreign invader. As discussed above, molecular mimicry can occur, where antibodies cross-react with your tissues, or a chronic low- level immune response can occur, leading to chronic inflammatory states and immune imbalance. The best test for determining whether you have Leaky Gut Syndrome is the Cyrex GI Permeability test.
Various bacteria and viruses have been implicated in causing or contributing to Hashimoto’s in susceptible people. Viruses, including Rubella, Rubeola, Epstein-Barr (mononucleosis), Retroviruses, Influenza, and Coxackie have all been implicated. Species of the Yersinia bacteria genus can cause GI infections and have been connected to Crohn’s disease, arthritis and thyroid autoimmunity.
Iodine and Hashimoto’s
There is controversy among various thyroid experts on the role of iodine in autoimmunity. Dr. Datis Kharrazian cites evidence that iodine is contraindicated in Hashimoto’s, stating that it stimulates the production of the enzyme TPO, which is the most commonly attacked enzyme by antibodies in autoimmune thyroid disease. He notes that iodine can increase an autoimmune response in those with elevated thyroid antibodies. He also cites several studies that link increased iodine intake from supplementation, with iodized salt with increased autoimmunity.
Other authors (Brownstein, Starr and Abrahams) are of a different opinion. Dr. Starr in his book “Hypothyroidism Type 2” notes that Hashimoto’s patients who are gluten sensitive do not do well on iodine, until gluten is removed. He uses sea salt and small doses of iodine initially.
Dr. Brownstein in his books on iodine and thyroid disorders states that iodine deficiency predisposes the thyroid to oxidative damage and that the body’s defense against this is the production of antibodies. He uses iodine in addition to other antioxidants to reverse the oxidative damage.
Dr. Guy Abraham is the most vocal proponent of the use of iodine with Hashimoto’s. He notes that one of the research studies performed in 2006 that cited a positive association with iodine and autoimmunity, was retracted a year later by the study’s authors.
Dr. Abraham noted that Lugol’s Solution, which combines inorganic iodine and iodide had been used long before iodized table salt, in quantities up to 100 times the amount of iodine found in table salt, with no evidence of increased risk of Hashimoto’s. He notes that Hashimoto’s cannot be recreated in lab animals using inorganic iodide, unless goitrogens (antithyroid drugs) are added. He proposes that goitrogens combined with an iodide deficiency is the underlying cause of Hashimoto’s. He states “ Inadequate iodide supply to the thyroid gland, aggravated by goitrogens, activates TPO system through elevated TSH, low levels of iodinated lipids, and high cytosolic free calcium, resulting in excess production of hydrogen peroxide”. He notes that elevated hydrogen peroxide then damages TPO enzyme and thyroglobulin, which elicits an autoimmune response. He cites a study showing that iodide at concentrations that would be achieved by taking 50-100mg./day actually protected the thyroid from oxidative damage. He also discusses research that shows that patients with Hashimoto’s have significantly lower concentrations of iodide in their thyroid glands than do patients without Hashimoto’s.
Comments: Iodine deficiency is prevalent, with about 1/3 of the world being deficient. It is absolutely essential to life and good health. Some research shows that iodizing salt stops overt iodine deficiency but at the same time increases Hashimoto’s. Other research, cited by Dr. Abraham contradicts this. So which is correct?
In the studies that show that iodized salt relieves iodine deficiency, there are two issues. First is that the individuals given the iodized salt were already iodine deficient, which sets them up for oxidative damage as well as failure of delta iodolactone to be created due to lack of iodine. The small amount of iodine present in salt would be insufficient to iodize delta iodolactone. This would then not allow for proper cell signaling for cell differentiation and normal programed cell death of abnormal cells (apoptosis). Giving a small amount of iodine could then increase the production of hydrogen peroxide, without providing adequate protection against oxidative damage. Additionally, it is probable that the test subjects were also deficient in a number of other antioxidants, such as selenium, which are critical in protecting the thyroid.
The fact that the countries with the highest intake of iodine (Japan and Iceland) do not have the highest rate of Hashimoto’s speaks against iodine causing the condition. A typical Japanese diet provides up to 100 times the amount of iodine found in iodized salt.
In the USA, iodized salt was introduced in the 1920’s, in small quantities, which was sufficient to prevent overt goiters. In the 1960’s salt was credited for causing high blood pressure, and the use of iodized salt has decreased. In addition, iodine was removed from baked goods and replaced by bromide (an iodine antagonist and thyroid toxin). The average daily intake of iodine has been reduced by 50% since then, however the incidence of Hashimoto’s has not declined. If Hashimoto’s were caused by iodine, one would expect the frequency to have declined rather than increased.
The prudent course of action for patients with Hashimoto’s would be to first determine whether an iodine deficiency exists, by performing an iodine loading test. Before introducing iodine, providing a full array of antioxidants, including Vitamin C, selenium, magnesium and stimulators of the body’s own antioxidant systems should occur, followed initially by low-dose iodine, with frequent monitoring of antibody levels. This approach makes more sense than encouraging an iodine deficiency, with all the potential serious health issues that would occur.