Hypothyroidism and Hyperparathyroidism

Paul L. Reller L.Ac. / Last Updated: August 03, 2017


How Hypothyroid Conditions Occur

A variety of causes are known for Primary Hypothyroidism, including autoimmune dysfunction, postpartum thyroiditis, viral illness, more than a few drugs (Lithium, interferon alpha, thalidomide, amiodarone (antiarrhythmic), stavudine (antiviral), proton pump inhibitors (acid reflux), tyrosine kinase inhibitors (chemotherapy drugs), steroids, sulfonamides (a large class of drugs that includes antibacterial, anti-diabetic, diuretic, anticonvulsant, anti-inflammatory, and protease inhibiting drugs), and excess radiation exposure (CT scans, cancer therapy, radioactive iodine), but iodine deficiency is by far the most prevalent factor, often aggravated by the increased number of halides in the environment, such as bromide, fluoride, chloride and astatide.

These halides, in the same charged mineral class as iodine, compete with or inhibit absorption of iodine, and contain known goitrogens. Persistent halogens in the environment from pesticides and flame retardants, such as DDT, PCB, PBB, BDE, and PBDE, many of which are now banned from production but do not break down in the environment, are accumulating in human tissues. While the manufacturers of these industrial halides or halogens continue to claim that low levels of these chemicals pose no known risk, they are aware that they do not break down in the environment, are ubiquitous, and thus gradually accumulate in the human organism to reach the level of health risk and harm. In addition, these manufacturers know that studies that isolate each of these hundreds of widely used halides or halogens to evaluate health risks purposefully ignore the fact that these chemicals should be grouped in studies to evaluate accumulative harm. Proton pump inhibitors (acid reflux) such as Prilosec and Nexium are popularly prescribed and may be a contributing factor in many cases of hypothyroidism. Many cases are considered multifactorial, meaning that a variety of health factors may combine to cause the hypothyroidism, and the long and complicated list of contributors to subclinical hypothyroidism makes this problem difficult to deal with for most individuals. The way to deal with complicated issues is to take it one step at a time, though, and iodine deficiency is a good place to start for many people. In recent decades in the U.S. population studies have noted a high prevalence of iodine deficiency in certain geographical regions and especially in women approaching menopause, making this nutritional deficiency once again an important consideration. When the body struggles with iodine deficiency, increased TSH (thyroid stimulating hormone) is produced to compensate. High TSH levels with normal circulating levels of active thyroid hormones is the diagnostic criteria for subclinical hypothyroid disorder and this could potentially be solved simply by taking an iodine supplment. Understanding iodine physiology helps to put this often confusing public health problem into perspective.

Iodine is an abundant earth mineral that forms the backbone for thyroid hormones. Without sufficient iodine, our thyroids cannot produce sufficient thyroid hormone. A normal diet should contain 400-500 micrograms of iodine per day, and the thyroid gland should take up about 80+ micrograms daily. Once dietary intake of iodide is consistently under 100 micrograms per day for a period of 3 months, hypothyroidism will occur progressively. Iodide is the reduced form of iodine in the body, where an extra electron is added. The World Health Organization (WHO) now warns that about 1/3 of the earth's population lives in an area of iodine deficiency. Iodine deficiency in the past was seen in areas very far away from the ocean, and in mountainous areas, but today, most iodine depleted areas in the world occur in highly industrialized societies such as the United States. Not only iodine deficiency, but ability to utilize the iodine is important, and mineral balance, with partner minerals such as selenium, is also important in maintaining the most basic requirements of healthy thyroid hormone production. Magnesium may also be deficient and create problems with iodine utilization, as well as the creation of excess H2O2 from activation of thyroid peroxydase (TPO) due to excess cytosolic calcium. While a number of factors may contribute to hypothyroidism, we should not overlook the basics, such as supplying the body with the right nutrients to produce our most important hormones.

Like calcium, iodine is a mineral that was produced in abundance when the planet was covered in saltwater, and animal life was living in this mineral-rich saltwater. As we evolved onto land, our bodies stored this mineral-rich saltwater inside the body, and even today, a normal saline solution is the basic component of our blood and extracellular fluids. Saline refers to salt, not sodium, and a salt is a chemical compound that reacts to an acid-base interaction where charged ions in acids are replaced by mineral ions from bases. Salt from seawater is deposited over the globe and contains a specific balance of about 60 minerals, including abundant iodine, while the food industry has tried to define salt as simple sodium chloride. Commercially produced salt as simple sodium chloride resulted in a large number of cases of hypothyroidism in the first half of the twentieth century in the U.S. and was partially corrected by adding iodine to table salt, bread, water and other products. Iodine was deposited in the soils of the world when the seawater receded, and gradually enters the foods we eat. In some parts of the world, there is much less iodine in the soil, and these areas have much higher rates of thyroid deficiencies, often manifesting as goiter. This problem was solved historically by importing natural sea salt to the population. As modern industry and farming methods developed, soils were depleted of iodine. While the subject of iodine depletion in our environment, and subsequent iodine deficiency, has not been a popular public topic since the early twentieth century, it is obvious that over time environmental iodine depletion is likely to worsen in the environment. The ability of the human organism to adapt to less iodine may not proceed as quickly as this depletion, especially as a number of industrial factors accelerate the environmental iodine depletion. The signs of nutritional iodine deficiency are slowly apparent, and as iodine stores in the body, the depletion may reach a points where thyroid dysfunction starts to occur on a gradual basis. There is no sense to ignoring this history of iodine deficiency as a cause of hypothyroidism, and no sense in dumbing down the situation, yet this is what has occurred.

In the first part of the twentieth century, areas of the United States around the Great Lakes produced a high incidence of goiter and hypothyroid conditions. Treatment with iodine was developed, and this problem was dramatically reduced. Iodine was then added to common table salt by government regulation to help insure that a sufficient daily intake was achieved. In recent decades common table salt had been depleted of minerals such as iodine by commercial processing, though. Sea salt will naturally have abundant iodine, and is a healthy alternative to commercial table salt. Iodine was also added to commercial breads in the past to achieve sufficient daily intake in the population that did not have a healthy diet. Unfortunately, iodine was removed from commercial breads and bromide was substituted around 1970. Since bromide inhibits iodine assimilation in our bodies, and since bromide is now added to our drinking water, this presents a significant added problem to dietary iodine intake. It is no coincidence that rates of autoimmune and subclinical hypothyroid conditions increased after 1970. By ignoring these concerns, the FDA has created an enormous health problem. Bromine is one of a group of chemicals, that includes iodine and fluoride, called halogens, which compete in our bodies. Since these chemicals compete in the body, increasing bromine and flouride presents a problem of deficient iodine assimilation that hasn't been addressed. Today, pesticides, fumigants, flame retardants, and antibacterial agents that all contain bromine have been used more and more extensively in the United States. Fortunately, the EPA is finally proposing lower acceptable amounts of fluoride in the water supplies, but much more needs to be done to insure public health benefits.

In January of 2011, the U.S. Dept. of Health and Human Services announced that it is lowering the recommended levels of flouride in water to 0.7 mg per liter, the first change since 1962, although many scientists have suggested this move for quite some time. The E.P.A. is also reviewing whether the allowed maximum for fluoride in water of 4mg per liter also be lowered. The longstanding standard for fluoride in water has been 0.7 to 1.2mg per liter. Now, the news media is reporting that this move is because of concerns that too much fluoride causes spots on children's teeth between the ages of 1 and 4, (re: NY Times 1/7/2011 article in the Politics section entitled Government to Recommend Less Flouride by the Associated Press). Now, high fluoride has been shown to cause a metabolic alteration in the ameloblasts of developing teeth, resulting in defective matrix and improper calcification. This is the prevalent, but unproven theory, since fluoride levels are dependent on a number of factors, including kidney excretion. According to these theories, though, a liter of fluoridated water with 1.3 mg per liter of fluoride per day would be necessary to cause mild tooth discoloration in a child 1-4 years of age, and preclude the developing teeth to mild discoloration. For persons over 9 years of age, 10 liters of water per day at 1 mg of fluoride per liter would need to be drunk to cause mild tooth fluorosis. These amounts of tap water are not consumed, and this is not a reason to lower fluoride levels. Obviously, fluoride levels were lowered because this is linked to excess halogens leading to deficient iodine. The pervasiveness of downplaying potential iodine deficiency and its many causes is astounding.

The actual reasons for the limiting of fluoride by the Dept. of Health and the EPA is because fluoride is a halogen, and the number of halogens competing with iodine in the environment is getting dangerously high, contributing to iodine deficiency, and that accumulation of fluoride in brain tissue can reduce synthesis of melatonin, and possibly affect other hormones. Excess fluoride, and bromides, inhibit iodine absorption, resulting in defective thyroid and parathyroid metabolism, and consequently poor hormonal regulation of calcium deposition in teeth and bone. Numerous studies have shown that excess exposure to fluoride can cause osteosclerosis as well (Rich, Ensinick and Ivanovich; Univ. of Washington, Journal of Clinical Investigation Vol.43;(4)1964). Studies have found that relatively low doses of fluoride may depress resorption of bone (release of calcium from the bone to circulation as needed). The U.S. National Research Council has stated that "several lines of information indicate an effect of fluoride exposure on thyroid function", particularly among individuals with an iodine deficiency. Medical doctors once used fluoride to reduce thyroid activity in hyperthyroid patients (see the link in Additional Information on this subject). The most important health reason for a lowering of fluoride in drinking water is that excess halogens such as fluoride and bromide in the environment are a threat to iodine levels in the body, and subsequently the development of hypothyroid disorders, hyperparathyroid disorders, breast and other cancers.

In the last thirty years, iodine deficiency has worsened, as farming methods have ruined our topsoils and removed the mineral rocks from the soil. Common commercial table salt has decreased in quality, with production methods decreasing its ability to hold usable iodine. The National Health and Nutrition Survey (NHANES) showed that dietary iodine levels in the United States declined 50% between 1971 and 2000, as noted by the Centers for Disease Control (CDC)! Since iodine is an important antioxidant that protects against breast cancer, ovarian cancer, prostate cancer, and thyroid cancer, the rise in incidence of these problems, as well as subcinical hypothyroid states, is logically linked to declines in dietary iodine. Iodine stores in these tissues, and a depletion of tissue iodine stores contributes to various protein dysfunctions that are directly linked to increased cancer risk as well. As early as 1918, researchers found that increasing iodine to laboratory animals also decreased atherosclerosis, and Iodine is a potent alkalinizing agent, and so declines could also account for increases in metabolic acidity. Since 2000 there has been an explosive growth in the use of glyphosate herbicides, such as RoundUp, widely marketed to match with a set of genetically modified staple food crops (GMO), and glyphosate is a strong metal chelator, creating even more mineral deficiency by binding the natural minerals in soil and preventing them from getting into our food crops! In 2013, experts at MIT (Massachusetts Institute of Technology) released a study that showed that glyphosate herbicides contribute to thyroid disease by reducing essential mineral availability in food (Samei and Seneff, Interdisciplinary Toxicology 2013 Dec; 6(4): 159-184). All of these potential health risks from gradual iodine deficiency are not directly tied to hypothyroidism, but obviously contribute to the complex symptom presentation in subclinical hypothyroid conditions.

In the past 20 years, numerous population studies across the country have noted areas where over 90 percent of the population was deficient in iodine! This fact is being stubbornly ignored. While this is not the only reason why people develop thyroid deficiency, it is the most basic reason. In the last 10 years there is a growing number of M.D. specialists that are revisiting iodine supplementation as part of a treatment protocol. When this started, the industry, as it did with popular and effective herbs, published reports of alarming risks from iodine supplementation. As intelligent professionals looked at the risks, and studied this problem, the ruse was very evident. In the early half of the twentieth century, iodine supplementation with Lugol's Solution (established in 1829) was very prevalent. This iodine supplement was widely available at most apothecaries without a prescription, and was used for a very wide array of health problems. Before modern pharmaceuticals took hold of the market, this was perhaps the most widely used medical item in the world. If iodine produces so much risk, where is the data from the past that supports this assumption? There was some concern and scientific study by the Mayo Clinic of a rise in the incidence of Hashimoto's thyroiditis after the introduction of iodine in our food in the early half of the twentieth century, but this extensive study concluded that iodine supplementation was not the cause. In recent years, Western pharmaceutical concerns helped form a Chinese review of these studies, with the initial conclusion by Wang et al indicating that iodine supplementation could cause thyroiditis, but after challenge, the authors acknowledged that a 'faulty' study design was responsible for this wrong conclusion from the data of the Mayo Clinic studies. Repetition of these warnings of the use of Lugol's Solution (Iodoral) are prevalent in standard medicine despite the studies that clearly repudiate these dangers. You may find the sound scientific studies in Additional Information at the end of this article, with links to the studies. We may assume that the systemic repetition of false data are industry lies intended to reinforce the discouragement of this safe and simple treatment to increase sales of synthetic thyroid hormone.

There are some patients that will have an adverse reaction to a high dosage of iodine supplement, though. Modern studies have shown that in the subset of the population that may acquire autoimmune Hashimoto's thyroiditis, that about 19% of these subjects have an allele (half of a gene expression) that could allow a deficient thyroid to accept too much iodine and cause a hyperthyroid state. Subsequent studies have shown that this is an easily reversible problem that produces no permanent problem, though. Signs and symptoms of sudden hyperthyroidism are clear, and in these cases, supplementation should be stopped, and a lower dose and increased dietary iodine should be tried. Since there are a number of nutritional deficiencies that could account for poor utilization of iodine, supplementing with magnesium, selenium and Vitamin C before resuming a higher dose iodine (Iodoral) is recommended. For these patients, monitoring by a professional is important when taking the iodine supplement, and starting with a low dose and gradually increasing the dose is also important. Since iodine stores in the body, long-term supplementation should not be constant. The fact that so many common nutritional supplements and mineral packages now contain iodine is a clear indication that this period of untrue alarm concerning iodine is over. Of course, for most people, increasing iodine in the diet and decreasing commercial food products, eating natural high quality sea salt, and decreasing the amount of tapwater drunk (fluoride), will restore levels of daily iodine in the diet. Occasional use of an essential mineral supplement containing iodine could be helpful as well. Gradually, as the iodine stores get back to normal, the thyroid metabolism may also be restored. If this does not work, a professional medical analysis of the potential problems that could inhibit iodine metabolism is recommended, and a step-by-step restoration of homeostasis tried. No matter what the outcome, the increased intake and storage of iodine has many health benefits, and presents no dangers. The only real danger of professional iodine supplementation is the potential decreased need for pharmaceutical synthetic thyroid hormone T4 (levothyroxine or synthroid). Hopefully, in many patients, this therapy could restore a normal thyroid homeostasis and function (an euthyroid state).

Inflammatory dysfunction and onset of hypothyroidism

Chronic inflammatory states and various inflammatory mediators have been linked to hypothyroidism and hormonal balance. Cytokines are inflammatory mediators excreted by all cells that coordinate the inflammatory mechanisms needed to clear infection and promote healthy tissue repair and maintenance. Cytokines are proteins, peptides or glycoproteins, and may have an effect as both a paracrine and endocrine, meaning that they may play a significant role in hormonal health directly. One of these common inflammatory mediators is interleukin-6, and a link below under additional information will elucidate how this inflammatory mediator plays an important role in overall hormonal balance, and may be excessively secreted by our cells in response to both physiological stress and excerbated by chronic hormonal deificiencies. For many years, we have assumed that these interleukins only play a part in inflammatory responses, antibody generation, and blood cell production, but we now know that excesses of such chemicals as interleukin-6 may significantly alter the hormonal balance and lead to hypothalamic and thyroid imbalance. Various autoimmune disorders result in excess levels of interleukins, and this has led researchers to seek the connection between autoimmune disorder and hypothyroidism.

One important aspect of inflammatory health that has been linked to both autoimmune disorders and hypothyorid states is celiac disease, or the chronic overproduction of antibodies in the gut in response to the allergic hypersensitivity of food glutens and gliadins. This problems increased exponentially when the food industry adopted the common use of high gluten flours to create faster rising times and save money in commercial food production. Any food chemical stimulates some antibody response in our bodies as a means of protection, but when we suddenly inflict high concentrations of these food chemicals in the general diet, many people will respond with an excess antibody response. Gluten and gliadin sensitivity creates a chronic excess IgG response in the intestinal lining and excess secretion of interleukins, which is termed celiac disease. This is one of the potential causative factors in subclinical hypothyroidism. Atypical celiac disease, allergies to glutens, and hypersensitivity to glutens without celiac disease may also occur, and affect hypothyroidism. A 2012 study at Sapienza University of Rome (cited below in additional information) found that in patients diagnosed with Hashimoto's thyroiditis, that the occurrence of atypical celiac disease actually increased the need for the inactive thyroid hormone T4, or the synthetic thyroid T4 levothyroxine. This affect was reversed by gluten avoidance or resolution of the atypical celiac disease, and was attributed to malabsorption of the T4 medication. A 2006 study by the Mayo Clinic showed that patients taking a dosage of Levothyroxine (Synthroid) of greater than 125mcg had a high incidence of abnormal TSH levels, while those taking less than a 125mcg dose had greater control. Resolution of problems with malabsoprtion of synthetic T4, clearing of chronic immune inflammatory stress, and gentle stimulation of better normal thyroid function with CIM/TCM could at least insure that the necessary dosage of synthetic T4 was lower.

We see that problems with the health of the gastrointestinal tract and difficulties digesting proteins may affect hypothyroidism in a number of ways, contributing to immune dysfunction, chronic inflammation, malabsorption of drugs, and adrenal stress. Such information allows the holistic physician to offer an array of advice and treatment to the patient to address the role of inflammatory dysfunction in the hypothyroid syndromes, and resolve the underlying problems with the gastrointestinal tract, difficulties with digesting proteins such as glutens, and the inflammatory dysfunction that accompanies such states. To read more about celiac disease and gluten-related pathologies, go to the article on this website entitled Malabsorption Syndromes and Celiac Disease, Gluten et al. Periodic courses of acupuncture with an individualized step-by-step course of herbal and nutrient medicine could address any of these contributing problems and improve the overall treatment and quality of life.

Other endocrine imbalances that may be related to Hypothyroidism

Since the thyroid is the key regulatory hormonal gland in the endocrine system, and the hormonal endocrine system is a complex feedback system, other imbalances in this system will create or contribute to thyroid dysfunction. The main axis of feedback regulation is called the adrenal pituitary axis (HPA axis), but this does not represent the entire system of endocrine regulation by any means. Complete, or holistic, hormonal balance is the key to a healthy thyroid function. In the brain, our neurological system plays a key role as a partner to the hormonal system. Neurohormonal imbalance is increasingly studied and is found integral to a wide variety of disease states. We are all aware that nervous stress affects the hormonal balance, as many women are affected by nervous stress and increased premenstrual symptoms, as well as menstrual irregularity and dysmenorrhea (dysfunctional bleeding causing cramping pain). Thus, neurohormonal balance is a key factor in maintaining healthy thyroid function. Insulin is a hormone that is also highly associated, and as many as 25% of post-partum women with Type 1 Diabetes, an insulin disorder, experience post-partum hypothyroid disorder. Women with insulin resistance and sluggish insulin response may experience higher risk. All of the steroid hormones are closely related, pregnenelone, testosterone, cortisol, progesterone, the 3 types of estrogens, and insulin, and all work within a complex feedback homeostasis that needs to be maintained at an optimal level. Taking synthetic hormones will result in lower levels of natural hormones being produced, and use of hormonal contraception, hormone replacement therapy in menopause, and synthetic thyroxine may all have a negative effect on the whole system, even if they work well to relieve some symptoms.

The array of health problems that is associated with thyroid imbalances is large. The list includes parathyroid problems, adrenal insufficiency, diabetes or metabolic syndrome, hypertension and hypotension, infertility, coronary artery disease, obesity, candida overgrowth, arthritis, osteoporosis, ovarian cysts, endometriosis, PMS, fibrocystic breasts, cancer, chronic fatigue, allergies, mental disorders, multiple sclerosis, psoriasis, gout, and other autoimmune disorders. The Colorado Thyroid Disease Prevalence Study examined 25,862 persons and found that 10 percent had an undiagnosed abnormal thyroid function. In 2004, the Journal of Clinical Endocrinological Metabolism published a study that found a 260% increase in the prevalence of heart disease with subclinical hypothyroidism as well. Elevated TSH was found to exert both direct and indirect effects on the arterial health. The scientific study of the potential harm from thyroid imbalance, and endocrine imbalance in general is large and cannot be ignored.

Children born of mothers with subclinical hypothyroid conditions have been found to have increased incidence of attention deficit and hyperactivity disorders, problems with memory and sensorimotor skills, abnormal visual processing, and lower IQ. Infants that inherent a hypothyroid condition exhibit neurodevelopmental problems, and one study found that 10% of children whose mothers had a low T4 count at 12 weeks scored significantly worse on the Psychomotor Developmental Index compared to other children (Clinical Endocrinology, Oxford; 2003:59:282-8). Maintenance of thyroid and hormonal balance is important to future generations, and has been found to be a significant contributor to the increase in ADHD in children today.

Incidence of osteoporosis in later life has also been linked to thyroid hormone deficiency during pregnancy, as well as transient hypothyroid states during childhood development. Studies have indicated that either a deficiency of TSH (hypothalamic deficiency or dysfunction) or T3 (active thyroid hormone) may be a causative factor in onset of osteoporosis later in life. Studies on animals found that thyroid receptors may be altered by hypothyroidism during pregnancy, and mutations of the thyroid receptors may be exacerbated by transient periods of hypothyroidism. Normal thyroid states during development are required for establishing normal adult bone structure and mineralization (J.H. Duncan Bassett et al, Clinical Sciences Centre, Imperial College London; Molecular Endocrinology 21(8);1893-1904;2007). This information leads us to the conclusion that attention to endocrine balance is important in the female population, both to prevent hypothyroid pathology, but also to insure fertility and health of the offspring.

This information leads us to one conclusion. Preventative medicine and holistic medicine is essential to the population as it ages, especially the female population. Waiting until the allopathic medical system diagnoses a clinical thyroid condition and then taking a synthetic thryoid medication is not sufficient to insure overall health. The intelligent patient integrates Complementary Medicine into their healthy regimen to insure that risk of all of these common health problems and diseases is kept to a minimum. As we see from this article, Complementary and Integrative Medicine (CIM/TCM) may be utilized in a variety of ways to insure better health and long-term outcomes, or relieve specific symptoms of the disease. The choices in treatment protocol, and the goals of treatment, should be the choice of the patient, and gaining a greater understanding of the disease, and the variety of treatment options in CIM/TCM is essential for the best results.

Hypothyroidism secondary to autoimmune Hashimoto's Thyroiditis

Hashimoto's thryoiditis is a complex disease that was the first to be recognized as an autoimmune disease. Hashimoto's is thought to be the most prevalent cause of clinical hypothyroidism in the United States, affecting more than 1.5 per 1000 in the population and occurring in women 10 to 20 times as often as in men. The prevalence of the autoimmune disease is seen primarily in women between the ages of 45 and 65. In Hashimoto's thyroiditis, a variety of autoimmune processes, involving a variety of antibody responses, is seen, making this disease variable from one patient to another. Antibodies to thyroid peroxidase (TPO) and thyroglobulin in the thyroid gland, and thyroid stimulating hormone receptors (TSHR) on the surface of the thyroid follicles, have all been associated with Hashimoto's. Antibodies do not show a high affinity for TSHR, leading some scientist to question whether the receptors need to be activated by another disease process to incur the autoimmune response. Mutations of the TSH receptors are seen and implicated in a number of diseases, and may be related to various disease mechanisms. More than 30 TPO mutations have been identified in scientific research, many or which prevent TPO from assisting thyroglobuin in the creation of thyroid hormones and the uptake of iodine necessary to create thyroid hormone. Since there are so many genetic mutations involved in this one aspect of the disease, it is highly unlikely that biotechnology will create a single drug to reverse all of the genetic expressions linked to the disease. A more complex holistic approach to treatment is logically necessary.

Because of the complexity of the disease, the term Autoimmune Thyroid Diseases is now used to describe the problem, instead of the term Hashimoto's thyroiditis. The eventual and gradual atrophy, and even destruction, of thyroid gland follicles often occurs due to indirect imbalances in the thyroid and inability of the follicles to uptake iodine and create thyroid hormone. The patient and the physician needs to recognize the complexity of Hashimoto's and treat the various aspects of the disease, rather than focusing too narrowly on one particular aspect.

Typically, Hashimoto's Thyroiditis presents with a short period of hyperthyroid state, and then proceeds to a hypothyroid state. Sometimes, periods of hyperthyroid state may also occur in the course of disease. Modern medicine has treated by using synthetic corticosteroid to calm a hyperthyroid state, and then synthetic thyroid hormone to control the hypothyroid state. It is believed by many physicians that many of the hyperthyroid episodes may be due to improper stimulation with synthetic thyroid hormone as the body decreases its autoimmune reactions and repairs the various affected tissues. Many patients treated with these protocols experience a complex deterioration of health and seek a more comprehensive strategy from Complementary and Integrative Medicine. Despite management of the disease with synthetic thyroid hormone, a large percentage of patients experience other autoimmune diseases, such as Vitiligo's and Sjogren's, as well as hypoparathyroidism, adrenal insufficiency, and anemia. Graves' Disease, another thyroid autoimmune disorder that results in hyperthyroidism and thyroid nodules, is also related. Up to 23% of Hashimoto's patients may get cancer. Because of these risks preventative and holistic care is essential in the treatment protocol.

Symptoms that are specific to Hashimoto's thyroiditis include a feeling of fullness in the throat, painless thyroid enlargement (the thyroids are located on the sides of the neck, lateral to the esophagus, just below the Adam's apple in men, and nearly down to the collarbone, with the inferior portion larger), exhaustion, persistent sore throat, and possible low-grade fever. Often, though, these symptoms are transitory or mild, and go unnoticed. When an enlarged thyroid or thyroids are noticed, difficulty or discomfort swallowing, or hoarseness may prompt the patient to seek an examination. Since a number of presentations may result in an enlarged thyroid (goiter), it is very important to obtain a careful differential diagnosis before rushing into a specific course of therapy, especially a full bilateral thyroidectomy, which may not be necessary to correct the problem.

Initial symptom presentation when antibodies are detected may be minimal. Depression, weight gain, fatigue, sensitivity to cold, metabolic disorder, constipation, and other signs of slow metabolism often have occurred after a period of anxiety, mania, panic attacks, racing heart, weight loss, etc. Because of these presentations the diagnosis is often difficult and patients are assumed to be suffering from bipolar disorder, premenstrual syndrome, etc. This also points to the fact that there is rarely an immediate threat to health and survival from this disease, and plenty of chance to treat it with a holistic approach. The treatment must be individually tailored, closely monitored, and address all aspects of the disease, including symptom alleviation, elimination of possible causes, adrenal stress, deficient hypothalamic function, immune health, metabolic health, and specific autoimmune mechanisms. While this strategy is complicated, a step-be-step approach is simple, and not all of the available therapeutic protocols need be used at the same time. A goal oriented approach with short courses of acupuncture, and a step-bey-step persistent approach with herbal and nutrient medicine allows each individual to meet specific goals one at a time, and eventually restore health without a dependency on chronic use of the medicines. Herbal and nutrient medicine should be used to restore health, not replace it, which is the goal in allopathic medicine, using a chronic dependency on pharnaceuticals. CIM/TCM is not as profitable as allopathic medicine, but is a healthier approach.

One aspect of the disease mechanisms is the actual overexpression of white blood cells, or leukocytes, mainly T-cells, in the thyroid. These cells generally express and accumulate in tissue that is infected with a virus, or other pathogen. T-cells are also expressed in response to tumor cells, or older cells that experience excess cellular mutation and do not get cleared from the body by normal cell death, or apoptosis. Sometimes, these long-living T-cells may themselves become dysfunctional, either in creation, or in response to alteration during their weeks to years lifespan by deep viruses, retroviruses, or other toxins. Since the T-cell responses are part of a complex cytotoxic complement response in the body, we have also found a host of cells and receptors that may contribute to the excess T-cell responses in the thyroid. For example, there has been found a correlation between the percentage of antigen reactive Ta1+ T-cells and the level of anti-TSH receptor antibody. Research has found that Ta1+ T-cell activation may be causally related to T-cell receptor and CD-2 mediated mechanisms, particularly metabolic processes such as excess phosphorylation. CD-2 is an immune complement cell that is a glycoprotein that functions as a co-receptor in the T-cell response. Such metabolic problems as advanced glycated endproducts (AGEs), amino acid deficiencies, accumulation of protein fragments in thyroid tissues, poor antioxidant response, etc. may be implicated in the etiology and progression of Hashimoto's and subsequent hypothyroid state, and all of these health concerns need to be addressed in holistic analysis and treatment.

Genetic components are seen in about a third of cases, and are associated with major histocompatibility complex (MHC), a part of the human genome associated with autoimmune and immune responses, as well as non-MHC genes. Interactions between environmental factors and these genes is still poorly understood, but such factors as medications, infection, iodine variances, smoking and stress have been linked. For about 19% of Hashimoto's patients, one of the alleles of a gene in this complex may be responsible for triggering a hyperthyroid response to increases or changes in iodine. Iodine is a backbone of thyroid hormone, as well as a strong antioxidant in the thyroid, and deficiency is widely seen in the population, explaining a large number of hypothyroid cases and thyroid growths, such as goiter. This genetic component related to iodine is still poorly understood, but for a number of Hashimoto's patients, sudden increases in iodine supplementation may trigger a reversible hyperthyroid state. In these cases, the physician monitoring iodine supplementation will stop the iodine therapy and hyperthyroidism will quickly subside, with a euthyroid or hypothyroid state returning in short sequence, and no permanent consequences.

Iodine utilization may play an important part in the onset of Autoimmune Thyroid Diseases, and magnesium deficiency is thought to potentially affect this iodine utilization. Iodine is stored in the body, and the largest pool of stored iodine is in the thyroid. Iodine is essential to the formation of thyroid hormones and the attachment of thyroid hormones to carrying protein (thyroglobulin). The amino acid tyrosine is the backbone of the thyroid hormone molecule. Iodination of tyrosine residues by thyroid peroxidase (TPO) requires the presence of thyroglobulin, H2O2, and iodide. This system is inhibited by certain iodinated lipids and enhanced by free calcium ions in the cell cytosol. Excess cytosolic calcium may occur with magnesium deficiency and affect this metabolism. In autoimmune thyroid disease, the depletion of iodide could result in excess reactive oxygen species (ROS), or H2O2, affecting the TPO and thyroglobulin. The resultant oxidized TPO and thyroglobulin may then trigger an autoimmune reaction, especially in patients genetically predisposed. Magnesium deficiency is thus hypothesized to play a potential role in this process, creating excess cytosolic free calcium that encourages this metabolic dysfunction and immune response. Intracellular free calcium ions greater than normal may also contribute to calcification of cellular mitochondria and cell membranes. The cell membranes contain an ATP-dependent calcium pump that tries to maintain a physiologically normal level of free ionized calcium in the cell. This calcium pump is magnesium-dependent for normal function. Magnesium deficiency thus could potentially contribute to the pathology of autoimmune thyroid disease in two ways, causing an abnormal free calcium ion content in the thyroid cells, and excess calcification of the cell membranes and mitochondria. For this reason, many doctors who utilize Iodoral in clinical practice will first supplement with 800-1200 mg magnesium daily for a month before starting the larger iodine/iodide supplementation.

A part of the MHC, the human leukocyte antigen (HLA), is more strongly tied to the autoimmune thyroid diseases. HLA types are connected with a variety of diseases, including diabetes, Lupus, Sjogren's, Ankylosing spondylitis, Celiac Disease, Myasthenia Gravis, and myositis. These HLA alleles incur increased susceptibility to these diseases. In some cases, HLA mediated diseases are linked to cancers, such as gluten sensitivity enteropathy and Enteropathy-related T-cell Lymphoma. Normally, the HLA antigens are essential for healthy immune function, helping the body to identify both infected cells and cancerous cells, and stimulating destruction by T and B cells.

A variety of environmental factors and physiological stresses are probably the most important aspect of the Autoimmune Thyroid Diseases. Correcting these health imbalances may play an important role in reversing the genetic susceptibility to the autoimmune mechanisms. The patient should not overlook these factors and their importance in the overall treatment protocol. Hormonal imbalance, adrenal stress, deficient hypothalamic function, dietary problems, nutritional deficiencies, etc. may need to be treated for the immune therapy to achieve results.

All of the scientific study of Hashimoto's and hypothyroid states points to the lack of a silver bullet, or simple approach, to treatment, and the need for a comprehensive treatment protocol, perhaps utilizing a variety of physicians that may integrate their treatment successfully. The patient, in these circumstances, needs to become educated to the disease, and choose physicians and therapies that adhere to a systematic and sensible approach to treatment by addressing multiple problems in the body.

Problems with hormonal conversion in peripheral tissues

An increasingly prevalent problem noted as scientific research in hypothyroid dysfunction progresses is the noting of signs and symptoms of hypothyroidism when standard testing reveals no abnormalities. This is often due to problems of utilizing thyroid hormone in peripheral tissues. Circulating thyroid hormones include the inactive prohormone T4, and the active T3 (fT3). Our bodies convert the T4 to T3 as needed. A variety of problems may inhibit this T4 to T3 conversion. In this case, TSH and freeT4 (fT4) may be normal, but the action of the active hormone at the receptors may be deficient. One test that indicates that this condition is occurring is the reverse T3 (rT3) assay. If the rT3 is high, there is a problem with conversion of the T4 to T3 in peripheral tissues. Deficiencies of selenium and zinc methionine may account for the insufficient deiodinizing conversion of T4 to T3, whereas excess of cortisol and adrenaline may be responsible for excess deiodinizing conversion of T4 to rT3. Studies have shown that the now ubiquitous glyphosate herbicides such as RoundUp may inhibit the conversion of T4 to T3. Deficient active Vitamin D3 may also inhibit the T3 receptors, and supplementation with cholecalciferol D3 may be warranted. As stated, research has revealed that a significant number of patients with subclinical hypothyroidism have this problem of the peripheral thyroid hormone metabolism.Trying to solve these peripheral thyroid conversion problems by simply supplementing with methylselenocysteine, zinc monomethionine, hormone Vitamin D3 cholecalciferol high dose, and helping adrenal function and diurnal cortisol homeostasis with short courses of acupuncture, bioidentical adrenal cortex and cofactors, bioidentical pregnenelone, and use of a low dose melatonin at the same time each evening before bed could resolve these issue of peripheral thyroid pathology.

Causes of this condition also may include the nutritional deficiencies of iodine, iron, and Vitamins B6, B12, B2 and A. Medications that may cause this disorder include Beta Blocker hypertension meds, Birth Control pills, unopposed Estrogens, SSRI antidepressants, Lithium, Phenytoin (Dilantin for seizures), Theophylline, and Iodinated contrast agents used in testing and therapy. Contributors to this condition include smoking, excess alcohol consumption, aging, diabetes or metabolic disorder, fasting dieting, accumulations of lead, mercury or pesticides, excess stress, radiation, chemotherapy, fluoride, excess soy food products, adrenal insufficiency, hemochromatosis (a type of anemia), growth hormone deficiency, and deficiency of alpha-lipoic acid. We see from this extensive list why this condition is becoming more prevalent in our population. Sticking to an overly simplistic explanation of what causes hypothyroidism does not make sense, and only occurs because of the need to convince patients to just use a one-size-fits-all therapy with synthetic T4 levothyroxine and forget all the other Complementary and Integrative medical protocols that could benefit them. It is a certainty that many cases of subclinical hypothyroidism could be resolved by first diagnosing the condition accurately, and then trying to restore this peripheral metabolism at the thyroid hormone receptors. Many cases of clinical hypothyroidism that are not thoroughly diagnosed and assessed could also involve this peripheral dysfunction, and are thus misdiagnosed and the patients treated incorrectly with synthetic T4 for the rest of their lives, with inadequate overall outcomes.

When subclinical hypothyroid symptoms occur, this more elaborate treatment protocol and assessment could completely restore health and no further treatment would be necessary. Starting on synthetic thyroid hormone as T4 levothyroxine may temporarily relieve symptoms but in the long term many adverse health problems could occur that relate to chronic use of synthetic T4. While the full assessment and potential treatment protocols are not simple, the end result could be well worth the trouble, leaving one free of worry in the future about a host of health problems associated with both medication use and thyroid pathology.

Abnormal menstruation, infertility, and abnormal breast milk secretion with hypothyroid syndromes

Since hypothyroidism and hyperparathyroidism is often associated with hypothalamic dysfunction or deficiency, hormonal imbalances are frequently seen. Problems with normal secretion of luetinizing and follicle stimulating hormones (LH and FSH), as well as prolactin, from the hypothalamus pituitary system, may cause a variety of unwanted hormonal effects. When abnormal breast milk secretion is noticed (galactorrhea), the first diagnostic step is to examine thyroid hormones. Other neurohormonal balances may also contribute, as high prolactin, secreted from the pituitary when stimulated by the hypothalamus, is downregulated with dopamine, and upregulated with estrogens. High prolactin secretion can be caused by oral contraceptives and other synthetic hormone medications, especially unopposed estrogens such as Premarin and Depo-Provera, but a variety of medication toxicities could also be causing high prolactin secretion (hyperprolactinemia), including most anti-depressives and anti-anxiety agents, many hypertensive drugs, some stomach acid controlling medications, and the pain reliever Flexeril (muscle relaxant), as well as excess use of recreational drugs such as amphetamines, opiates and narcotics. Standard medicine has long place its emphasis on pituitary tumors, often overlooking these other common causes. The potential for a relative excess of estrogens in relation to a progesterone deficiency to cause or contribute to high prolactin metabolism is largely discounted and ignored.

Hyperprolactinemia, or high prolactin secretion, is becoming increasingly common in the U.S. population, and all of these problems, or causes, is obviously causing this higher incidence. Once again, the endocrine system is a complex feedback system, and restoration of endocrine homeostasis is the optimal solution to these problems. High prolactin causes decrease in luetinizing hormone (LH) and follicle stimulating hormone (FSH), which are also secreted by the pituitary and stimulated by the hypothalamus. Alterations in these hormones can cause infertility, irregular menses, amenorrhea, dysmenorrhea and premenstrual symptoms. Abnormal secretion of breast milk could be caused by hormonal imbalance associated with hypothalamic dysfunction, which could also cause hypothyroidism. Hypothyroidism with myxedema (deep swelling of tissues) could be a more direct cause in breast tissue. In any case, there is often a relationship between excess prolactin stimulation and hypothyroidism. Other signs and symptoms of hypothalamic pituitary dysfunction and hormonal imbalance that leads to high prolactin secretion include acne, abnormal facial and body hair growth, erectile dysfunction, breast enlargement, and decreased muscle mass. High prolactin is diagnosed with a simple blood test. A thorough diagnostic assessment should be performed when these symptoms such as menstrual problems become problematic. Unfortunately, standard medicine has been very resistant to this holistic assessment and treatment of hyperprolactinemia and these other hormonal imbalances, and rarely points out the relationship between these problems.