Hypothyroidism and Related Disorders

Paul Reller, L.Ac.

Hypothyroid syndromes include both clinical and subclinical types. The term clinical refers to a classic clinical disease presentation, but developing thyroid imbalances of a subclinical nature are now recognized as more prevalent, and present a variety of milder symptoms that reduce vitality, contribute to infertility, and present serious future health risks. Early treatment of subclinical hypothyroid conditions are highly recommended, and Complementary Medicine provides an ideal holistic approach that is supported by an ever increasing amount of scientific study.

While both presentations involve underproduction of thyroid hormones, clinical cases, indicating a defined symptomatic disease, involve alarmingly low levels of circulating thyroid hormones, while subclinical hypothyroidism may present as mild deficiencies or fluctuating thyroid hormone levels. The laboratory tests usually show high TSH (thyroid stimulating hormone secreted by the pituitary and stimulated by the hypothalamus glands in the brain) but normal freeT3 (active thyroid hormone not bound to a protein carrier) and freeT4 (inactive prohormone) in the circulating blood in subclinical syndromes. Sometimes problems at the peripheral receptors may present as normal TSH and T4, but deficient T3 and excess reverse T3. Because the circulating thyroid hormone levels are relatively normal in subclinical hypothyroidism there is little risk in utilizing a course of safe treatments with Complementary Medicine to try to resolve the symptoms and improve endocrine health. Restoration of the thyroid function often requires restoration of various aspects of the health, especially the endocrine, or hormonal, balance, and acupuncture, herbal and nutrient medicine provides an ideal therapeutic protocol for restoration of homeostatic balance. Some understanding of this complex physiological system and its problems is important in therapy, both for the acupuncturist and patient, and this article provides some useful clinical information.

Clinical hypothyroid conditions present more of a risk to the patient, as well as more severe clinical symptoms. Thyroid hormones play a vital role in regulating metabolic rate and tissue maintenance. Lowered metabolic rates present a variety of symptoms that decrease health and vitality, and cardiovascular risk is increased with poor tissue maintenance, as well as the reduction in erythrocyte glutathione, a key antioxidant and cell detoxifier. Since the endocrine system is a hormonal feedback system, any hormonal imbalance may affect the entire system and contribute to other hormonal imbalances, and a variety of hormonal pathologies are seen in clinical hypothyroidism over time. For example, osteoporosis and infertility are two problems of hormonal imbalance associated with hypothyroidism. Most cases of subclinical hypothyroidism gradually worsen, and usually go unnoticed, until this condition is suspected as the cause of another health problem, or because chronic anxiety, depression, and fatique become a persistent problem. Gradual inexplicable weight gain may also herald a diagnosis of subclinical hypothyroidism. Usually, we only know for sure if this condition exists by testing for levels of hypothalamic pituitary thyroid stimulating hormone (TSH), which should be tested along with a full thyroid panel, including the active unbound thyroid hormones in circulation, freeT3 and freeT4, SHBG (sex hormone binding globulin), TPO (thyroid peroxidase antibody), and levels of the adrenal hormones cortisol, DHEAS, and testosterone. I repeat this basic testing protocol because today, most institutional doctors are not testing for these various hormone parameters, opting instead to test only the TSH, and cheating the patient out of a full and comprehensive diagnosis and analysis of their problem. Testing for active hormone metabolites in saliva and veinous blood stick samples may be a more accurate and revealing test than simple test of circulating blood levels today as testing methods have improved in this realm.

In clinical hypothyroidism, thyroid hormones should be prescribed if the underlying condition cannot be resolved within a relatively short time frame. Since there are many potential causative factors in hypothyroid pathology, a holistic and thorough approach is needed with resolution of the underlying health problems. Synthetic thyroid hormone is almost always prescribed in standard medicine, but natural bio-identical hormones are finally gaining favor again, with the use of dessicated thyroid T3 showing much promise. This is an extract of animal thyroid hormone that is compatible with the human metabolism, and produces a bioidentical effect, with less side effects. One must search to find the M.D. with the knowledge to use this type of therapy, as most M.D.s are still guided by the wishes of the big pharmaceuticals to prescribe the more expensive patented synthetic medication, and use of natural T3 requires more attention and monitoring. Nevertheless, there are a growing number of M.D. endocrine specialists that are utilizing natural thyroid bioidentical hormone therapy, and work with an integrated approach that utilizes Complementary Medicine even when treating a more serious clinical hypothyroid condition. Complementary Medicine helps to restore hormonal balance, improve inflammatory regulation, and correct metabolic disorder that is at the heart of the thyroid dysfunction. As always, the first step is to get a thorough testing and differential diagnosis. Distinguishing the underlying causes and ruling out more threatening problems, such as cancer and nodular thyroid conditions, is important.

Poor thyroid function is often related to a broad endocrine imbalance, develops gradually, and presents as a subclinical, or less threatening disorder. Complementary Medicine offers an array of therapies, including acupuncture stimulation, herbal medicine, and nutrient medicine, that is backed by scientific study and is individually tailored to help restore thyroid and endocrine health.

In 1995, experts in thyroid disease from the University of Nebraska Medical Center conducted The Colorado Thyroid Disease Prevalence Study, where a cross-section of the public, namely 25,862 participants in a statewide health fair in Colorado, were assessed for symptoms, TSH levels, fT4 thyroid hormone levels, and lipid levels. The prevalence of elevated TSH levels in this population was 9.5 percent, indicating that nearly one in ten Americans may have a subclinical hypothyroid disorder, and the prevalence of a low TSH level was 2.2 percent. Among the patients already being treated and taking a thyroid medication, forty percent had an abnormal TSH level, indicating that standard treatment was insufficient to restore the endocrine health. Clearly, a more comprehensive and holistic treatment strategy is needed. More than fifteen years after this landmark study, standard medicine still has not adopted the needed changes. The study noted that elevations of TSH corresponded to changes in lipid levels that may affect cardiovascular health, and most cases of abnormal TSH did not produce symptoms that were alarming to the individual. Individual symptoms associated with thyroid disease were not a reliable indicator of disease, and often a number of symptoms were necessary to warrant the investigation of thyroid disease.

Numerous large population studies have been conducted since this landmark 1995 study, confirming a very high percentage of the populations with abnormal TSH levels. There has been little agreement worldwide on the implications, or even the definitions of differentiated thyroid disorders based on normal and abnormal TSH levels. The range of normal TSH is still controversial, and although studies show differences in the asymptomatic TSH levels with aging, the range of normal TSH has not been adjusted. A 2004 large study of the population in France (Valeix P et al: Annals of Endocrinology (Paris) 2004 Dec;65(6):477-86) found that among a representative population of 11,256 men and women, with patients previously diagnosed with thyroid disease excluded, that TSH levels of less than 0.4, indicating a subclinical hyperthyroid imbalance, were found in 7 percent of men, 5.3 percent of women aged 35-44, and 4.4 percent of women aged 45-60. The prevalence of subclinical hypothyroid imbalance as noted by TSH 4-9.9 were 11.1 percent of women aged 45-60, 7.2 percent of women aged 35-44, and 4 percent of men, with an additional nearly 1 percent of the population with a TSH greater than 10 mU/I, among the general population not diagnosed with a thyroid disease or imbalance. These studies conclude that it is still unclear whether this high percentage of the undiagnosed public is experiencing a biochemical imbalance or dysfunction, or a traditional thyroid disease. The French study concluded that a significant percentage of patients with abnormal TSH were affected by iodine deficiencies or other environmental factors (see study links below).

Subclinical hypothyroid conditions reflect a broad imbalance in hormonal health that onsets gradually and without significant symptoms, thereby going unnoticed. When the condition is discovered, it is usually because of routine laboratory testing, or because of generalized complaints of unusual fatique and low energy. There is mildly increased risk of cardiovascular disease over time with subclinical hypothyroidism, and the patient should address this unhealthy state to avoid stroke and heart attack. Many patients seek a simple treatment and opt for a single pill, while others wish to treat the condition by restoring hormonal health with Complementary Medicine. This latter group finds that improved health is worth the time and effort required with the holistic approach. Since there is usually no immediate health threat, these patients have time to explore and understand the various array of improvements in health that are needed to restore thyroid function.

Women with subclinical hypothyroid conditions present increased risk of cardiovascular disease, and over a 10 year period of time, increased mortality from heart attack, especially with aging, and with concurrent underlying cardiovascular risk, diabetic states, and autoimmune disorders. Men did not show this increased risk of cardiovascular mortality in studies, indicating that female hormonal imbalances were an important factor in associated health risks, and attention to the entire female hormonal balance is thus important to decrease future health risks. A full laboratory assessment should examine active metabolites of the sexual steroid hormones as well as the thyroid hormones, thyroid antibodies, cortisol levels, and even Vitamin D3 prohormone. The exact connection between the hypothyroid state and increased cardiovascular risk is still not known, although FSH has been shown to have a direct effect on the heart tissues and arterial linings over time. It could be that the same factors that lead to a subclinical hypothyroid condition also lead to an unhealthy cardiovascular state in women, though. The lesson to be learned is that the patient with these conditions needs to improve their overall health.

Symptoms and Signs of hypothyroid pathology

Subclinical hypothyroidism, like clinical hypothyroidism, is seen predominantly in women, with onset between the ages of 30 and 60, and may now be seen in at least 7-10% of the population. Symptom presentation often shows anxiety, depression, problems with cognition and memory, episodes of heart palpitations, difficulty in losing weight and elevated total cholesterol, although abscence of these symptoms does not rule out hypothyroid states. 5% of women after birthing acquire a temporary thyroid inflammatory disorder that usually first presents as hyperthyroidism and then often turns to hypothyroidism. A substantial number of these postpartum hypothryoid cases will become permanent without proper care. Clinical hypothyroidism symptoms include fatique, cold intolerance and chill, decreased ability to sweat, cool, dry skin, facial puffiness and sluggish movements. There is often a slowing of intellectual abilities and heavy menstrual bleeding.

Signs and symptoms of hypothyroid syndrome that are significantly more prevalent than in the normal thyroid population include dry skin, intolerance to cold, abnormal sweating, weight gain, coarse skin, puffiness, constipation, decreased bowel movements, numbness and tingling (paresthesia), cool skin, cold feet, hoarseness, hearing loss, and diminished ankle reflex. Of course, abscence of one or more of these symptoms and signs does not mean that you do not have a hypothyroid condition. Lowered basal body temperature is also a prevalent sign, and this can be easily monitored by the patient.

The thyroid gland is responsible for regulating organ functions, metabolic rate and calcium use. It is a key component of the endocrine system, which is a feedback system of regulation in the body. For this reason, a holistic approach to improve overall endocrine function is important. Since hypothyroid dysfunction may be caused by problems in the pituitary or hypothalamus, which are affected by nervous disorders, chronic pain syndromes, and hormonal imbalances, these aspects of your health must also be addressed in therapy. Subclinical hypothyroid syndromes are linked to chronic fatique syndromes, chronic viral illnesses, metabolic syndrome (diabetes), insulin resistance, menopausal imbalances and menstrual disorders. Restoration of function should address the whole endocrine system to some extent in most cases. Since the thyroid also produces other hormones, such as calcitonin, which works synergistically with parathyroid hormone to balance calcium regulation in the body, correction of subclinical hypothyroid dysfunction will prevent a host of other health problems. Calcium is the most highly regulated molecule in your body because it needs to be tightly controlled. Loss of calcium regulation is a serious health concern, since calcium is involved in many vital processes in your body. When symptoms of subclinical hypothyroidism are noted, it would be best to start treating early, and restore hormonal balance, before a host of serious related problems occur. Simple supplementation with calcium will not correct these problems, and eventually may do more harm than good.

Current testing and diagnosis of Hypothyroid disorders

Current testing and diagnosis of hypothyroid conditions has been inhibited by difficulties presented by insurance industry guidelines. Instead of a more thorough workup and specific diagnosis, most hospitals and clinics have curtailed the diagnostic workup, and often only the TSH (thyroid stimulating hormone) is now tested, or only TSH and the prohormone freeT4. This is because the pharmaceutical industry has not produced significant therapy over the last 50 years, relying almost completely on chronic prescription of synthetic thyroid hormone for all conditions. As the scientific information has increased, the treatment and testing has decreased. This is not an acceptable situation for many physicians and patients. Many scientific experts and journal in the last decade have described this as a health catastrophe.

In 2003, a report published in the British Medical Journal stated: “The biological effects of thyroid hormones at the peripheral tissues- and not TSH concentrations- reflect the clinical severity of hypothyroidism. A judicious initiation of (thyroid hormone) treatment should be guided by clinical and metabolic presentation and thyroid hormone concentrations, and not by serum TSH concentrations (alone).” A more thorough initial thyroid testing includes levels of TSH, freeT4, freeT3 (triiodothyronine, the active form of thyroid hormone), TPO (thyroid peroxidase antibody), and active Vitamin D3 (25-OH cholecalciferol). Hormonal values that are important in the diagnosis once a thyroid hormone imbalance is noted include diurnal cortisol levels, testosterone, DHEA-S, SHBG (sex hormone binding globulin), estradiol, progesterone, and PGE2 ratio, as well as reverse T3 (rT3). If a metabolic disorder is suspected, testing for triglycerides, fasting insulin, hemoglobin A1c, and High Sensitivity C-Reactive Protein (hsCRP) may be important to the overall treatment strategy. If anemia or kidney deficiency is suspect, testing for serum ferritin and B12, and a 24-hour urine test is warranted.

Patients may want to chart a basal body temperature, as this is highly associated with subclinical hypothyroid state. An electronic thermometer may be utilized for convenience, but if a standard thermometer is used, be sure to keep it at the bedside and shake it down before going to sleep. The basal temperature should be taken in the underarm, or axilla, before you have been awake and moving around for 10 minutes. Menstruating women should take the temperature on the 2-4 days of the cycle. Normal axillary temperatures range from 97.8-98.2F, but this range may vary in the population. To be sure of your range, ask the staff at your medical clinic to provide you with past measurements.

The reasons these tests are not conducted have little to do with cost. Currently, a complete and accurate profile is available with active metabolite testing, using saliva and bloodstick samples collected by the patient, and the total cost of a complete panel out of pocket can be as low as $300. The reason that the current allopathic medical system has reduced testing is to discourage information that can be utilized in a Complementary Medicine approach. The patient now needs to demand thorough testing and seek an integrative approach if they want to utilize a sensible holistic regimen.

How Hypothyroid conditions occur

A variety of causes are known for Primary Hypothyroidism, including autoimmune dysfunction, postpartum thyroiditis, viral illness, a few drugs (Lithium, interferon alpha, thalidomide, amiodarone (antiarrhythmic), stavudine (antiviral), proton pump inhibitors (acid reflux), tyrosine kinase inhibitors (chemotherapy drugs), etc.), and excess radiation exposure (CT scans, cancer therapy, radioactive iodine), but iodine deficiency is by far the most prevalent factor. Proton pump inhibitors (acid reflux) such as Prilosec and Nexium are popularly prescribed and may be a contributing factor in many cases. Many cases are considered multifactorial, meaning that a variety of health factors may combine to cause the hypothyroidism. 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. 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. 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.

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, 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.

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 as stated that “several lines of information indicate an effect of fluoride exposure on thyroid function&ldauo;, particularly among individuals with an iodine deficiency. Medical doctors once used fluoride to reduce thyroid activity in hyperthyroid patients (see the link below 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 Disase 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. 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% of the population was deficent in iodine. 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.

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 hyperthyriod state. Subsequent studies have shown that this is an easily reversible problem that produces no permanent problem. 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 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 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, will restore levels of daily iodine in the diet. 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.

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 hypothyrid 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. This is one of the potential causative factors in subclnical hypothyroidism. 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.

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, 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 insuline response may experience higher risk.

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 fatique, 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% 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. 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 thryoid 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.

Hyperparathyroidism and Hypothyroid syndromes

A growing incidence of subclinical hyperparathyroid disorder is also seen in the population, often associated with subclinical hypothyroidism and hypothalamic dysfunction. The parathyroid glands are small hormone excreting glands located on the sides of the larger thyroid gland. These glands predominantly secrete parathyroid hormone, a 84 amino acid protein, that is a key regulator of calcium and phosphorous. Activation of the stored preprohormone in the parathyroid, and release of the active parathyroid hormone in circulation, is dependent on a number of factors, including low concentration of calcium in the blood, concentration of phosphate in the blood, hypothalamic function, kidney and adrenal function, thyroid function, and parathyroid receptor function.

In a clinical primary hyperparathyroid disorder, the usual therapy is removal of the parathyroids, whereby other tissues in the thyroid start to produce parathyroid hormone and calcium phosphate levels are usually normalized. In recent years, minimally invasive approaches and partial parathyroid removal have been used and outcomes after 3 months appear to be the same for these procedures. Minimally invasive procedures locate the enlarged parathyroid glands and remove only these, using advanced scanning and ultrasound. Since the parathyroids are small and located usually on the sides of the thyroid, but sometimes in the interior of the thyroid, and sometimes away from the thyroid, locating the parathyroids correctly has been questioned in the past. Late-onset calcium deficiencies after minimally invasive parathyroidectomy has been noted in patients with Vitamin D3 deficiency, and monitoring with appropriate supplementation is recommended. Up to 40% of patients studied after parathyroidectomy develop elevated PTH levels but normal calcium levels in circulation, which is poorly understood, but appears to be related to kidney resistance to PTH mediated conversion of Vitamin D3 to its active hormonal form. While parathyroidectomy is considered safe and effective for both primary and secondary hyperparathyroidism, few studies have assessed quality of life in long-term outcomes. Some studies in Taiwan suggest that neuromuscular and neuropsychiatric abnormalities are common. Presently, these subjects are finally being explored. While parathyroidectomy is recommended and highly successful for primary parathyroidism, where an overstimulated parathyroid has become enlarged, it would be unwise to ignore the health problems associated with this condition, and many patients are now also seeking a holistic approach to restoring healthy hormonal balance after the parathyroidectomy, or minimally invasive partial parathyroidectomy.

Separating the thyroid from the parathyroid is a convenient simplification in modern medicine, but obviously, glands that are part of the thyroid gland do not function independently from the parent gland. In fact, in a significant portion of the population, the parathyroid glands are found inside, or part of, the thyroid gland itself. Parathyroid hormone acts only in balance with the thyroid hormone calcitonin, a 32-amino acid protein that modulates parathyroid hormone effects and is stimulated by both increases in circulating calcium and the stomach hormone gastrin. Because of this, both chronic intake of excess calcium supplement that is not quickly assimilated, and increases circulating calcium levels, and stomach dysfunction, which may alter calcitonin stimulation, may be implicated in parathyroid dysfunction. Hyperparathyroid dysfunction may be directly associated with chronic kidney dysfunction, Vitamin D deficiency (which is not actually a vitamin, but a prohormone), excess phosphorous in the diet (e.g. excess meat as a percentage of food intake), and chronic use of a thiazide diuretic to control high blood pressure, which may elevate circulating calcium. There is also speculation that chronic supplementation with calcium when there is poor calcium regulation may directly contribute to parathyroid dysfunction, especially when there is poor thyroid function, although high dose calcium carbonate has been used with some success to reduce PTH concentrations over time. More commonly, supplementation with D3 cholecalciferol is used in therapy, and some study of high dose D3 cholecalciferol is being conducted. Since D3 hormone is a potent regulator of calcium, this may reduce the need for parathyroid hormone and reduce stimulation of the parathyroids by the hypothalamus and pituitary.

The key to the connection between thyroid and parathyroid dysfunction appears to be the hypothalamus, a portion of the brain that signals the release of hormones that stimulate the production or release of other hormones. The hypothalamus thus regulates the activity, underactivity, or hyperactivity of the various endocrine glands, such as the thyroid and parathyroid. The hypothalamus is the common denominator. Much study has revealed a number of mechanisms by which the hypothalamus becomes deficient in function, as well as a number of nutrient medicines and herbs that stimulate improved hypothalamic function. Of course, if there is a nutritional deficiency, metabolic problem, or hormonal imbalance that is negatively affecting the hypothalamic function, this needs to be addressed to restore healthy function. Taking only one substance that may stimulate better hypothalamic function without correcting the other causes will not have a good overall outcome. This is why the comprehensive holistic approach is needed with Complementary Medicine. Scientific study also has shown that acupuncture stimulation may have a dramatic effect on hypothalamic function, and should be incorporated into the treatment protocol (see links to scientific studies below). Since the hypothalamus is also affected by the limbic system in the brain, which helps regulate mood and emotion, problems with emotional stress and control of anxiety and depression should also be addressed when needed. Such a comprehensive approach will produce long-lasting positive results over time.

Serum PTH (parathyroid hormone) is often seen at the upper limit of normal on blood tests in the targeted high-risk population, and so diagnosis of hyperparathyroid disease should be confirmed with confirmation of common symptoms as well as a full analysis of labs. Common symptoms included fatique, weakness, mild constipation, abdominal pain, changes in short term memory or cognitive function, depression, bone pain, osteopenia, increased urination at night, joint pain, and high blood pressure, although only some of these symptoms are seen in most individual cases. Lab tests should analyze circulating calcium, alkaline phosphatase, circulating Vitamin D3, phosphate and other electrolytes, and blood cell counts. Active metabolite tests may be run, analyzing Vitamin D3 metabolites, as well as a hormone and thyroid panel to gauge overall hormonal balance.

The parathyroid hormones along with the activated D3 hormone produced by the kidney are the main regulators of calcium in circulation (Vitamin D3 molecules, such as cholecalciferol, are the precursor, or prohormone, or preprohormone, to the D3 calcitriol). Calcium is the most highly regulated molecule in the body because it is large and a highly charged ion. There is abundant calcium in our bodies, in every cell, and much is stored in the bone matrix. Deficiency of calcium is perhaps not possible, although deficient calcium in the bone and in circulation is. When the calcium regulation is not functioning well, the patient may have excess calcium in circulation, or hypercalcemia. 90% of patients with hypercalcemia have hyperparathyroidism or a cancerous malignancy. Malignant cancer cells may produce a molecule that is very similar to parathyroid hormone, and excess may stimulate excess release of calcium from the bone. These parathyroid-like proteins have been increasingly studied in recent years and are found to compete at parathyroid hormone receptors, perhaps contributing to excess parathyroid hormone release in the abscence of parathyroid hypertrophy. In addition to hyperparathyroidism, thyrotoxicosis, or toxic inflammation of the thyroid, may also cause excess calcium in circulation. Adrenal insufficiency and chronic kidney dysfunction are also causes, as well as Sarcoidosis (granulatomatous disease), Vitamin A & D excess, and chronic use of the medications such as Thiazide diuretic, Tamoxifen and Lithium. All of these may contribute to a hormonal dysfunction and the Hyperparathyroid and Hypothyroid syndrome.

Besides calcium regulation, parathyroid hormone exerts a number of effects in the body. It regulates phosphates, stimulates and regulates synthesis of D3 hormone in the kidney, stimulates and regulates liver and blood cell proliferation, helps maintain mineral balance and acid-base balance, and is involved in immunoreactivity. Of course, it helps maintain healthy bones. There is also a relationship between blood pressure and parathyroid hormone, and indirect relationships with the health of brain cells and function. While all these hormonal mechanisms are still not well understood, the metabolism of the parathyroid, and the thyroid, are very important to overall health and well being. While modern medicine is still mostly concerned with primary Hyperparathyroidism and Hypothyroidism, and monitoring and treatment is geared almost entirely to severe problems and allopathic means of correction, the patient needs to pay attention to hormonal health and balance to achieve the best results when problems arise. To correct these problems, a more comprehensive approach is needed in Complementary Medicine. Don't expect that the treatment protocol will be as simple as taking a sythetic thyroid hormone or have the parathyroids removed. Expect to be proactive, learn about your body, and seek help to do all the things necessary to restore balance, or homeostasis.

The relationship between hypothyroidism and hyperparathyroidism has long been known. In a 1992 study at Loyola University, laboratory animals with induced elevation of TSH showed a 95% incidence of parathyroid hyperplasia, which would induce hyperparathyroidism. Despite these findings, there has been very little research focused on understanding this relationship. More research has been devoted to the relationship between deficiency of Vitamin D3 (which is not really a vitamin, but a prohormone), and both hyperparathyroidism and hypothyroidism. Deficiency of calcidiol, the active form or D3 hormone produced in the kidney, is a significant risk factor for the development of secondary hyperparathyroidism. Circulating levels of D3 are taken more frequently to assess this risk, and other risks. High dose supplementation with D3 cholecalciferol has created higher levels of calcidiol, but not as high as the patient might need. This implies that improved kidney and adrenal health is also necessary to restore this hormone imbalance. A combination of acupuncture stimulation, herbal therapy and nutrient medicine is ideal to achieve the best restoration of kidney function along with the taking of cholecalciferol to achieve a lasting effect on calcidiol. A 2005 study at the University of Auckland, New Zealand, Department of Medicine, found that replenishing cholecalciferol in hyperparathyroidism did not cause an increase in serum calcium, modestly reduced parathyroid hormone in circulation, as well as decreaseing bone turnover. How PTH was reduced by taking cholecalciferol was not well understood, underscoring how complex these interactions are in the hormonal system. Only be restoring hormonal balance can we insure that we get the healthy results that we are looking for.

An array of factors may be involved in the gradual imbalances in subclinical Hypothyroid and Hyperparathyroid syndromes, and these should be addressed in a comprehensive therapy

Environmental factors may also be playing a significant role in hypothyroid conditions. Researchers in 2006 discovered that a chemical commonly used in sunscreens called 4MBC mimicked the estrogen molecule and significantly raised the level of thyroid stimulating hormone in study animals, resulting in thyroid hypertrophy and deficient function. This chemical does not break down easily, and has been found by environmental researchers in the drinking water of many countries, and initial research has shown the potential for topically applied 4MBC to enter the bloodstream. Various estrogen-like chemicals used in common products, such as pthlalates in soft plastics, have also been linked to hormonal imbalances by researchers. While significant study on humans is not yet completed, the implications are alarming. These are just two common industrial environmental chemicals among a host of threatening chemicals that may cause or contribute to hypothyroid pathology. There may be more than one factor in the cause of hypothyroidism, and attention to potential environment causes should be considered in the overall holistic approach to restoring healthy function. These particular environmental links also show how estrogen imbalance is intricately tied to subclinical hypothryroidism, and how important healthy restoration of hormonal balance is to overall health in postmenopausal states or in women with menstrual problems.

A number of common industrial chemicals have been linked physiologically to thyroid dysfunction, including perchlorates, PCBs (polychlorinated biphenyls), PBDEs (polybrominated diphenylethers), BPA (bisphenol-A), organochlorine pesticides, and dioxins (see study citation link below). Perchlorates are used in the manufacture of military missiles, rocket fuel, airbags in autos, and flares, and these chemicals do not easily degrade in the environment. PCBs have been widely used in the manufacture of electrical transformers, capacitors, collants in refrigerators and many devices, plasticizers in cement and paint, sealants, hydraulic fluids, flame retardants, adhesives, wood floor finishes, de-dusting agents, water-proofing, surgical implants, and carbonless copy paper and do not decompose readily. PBDEs are widely used in flame retardants. BPA is used in the manufacture of soft plastics and epoxy resins. The EPA under the Obama administration is finally calling for a ban on many of these chemicals, but the accumulation in the environment will last for many decades, if not centuries. Mercury and lead organic compounds, which are common in the environment due to unregulated smokestack pollution from dirty coal electrical plants, smelters, and cement manufacturing, have also been definitively linked to thyroid dysfunction (see my article on these heavy metal toxins and the link to EPA reports on this website).

It is believed that the number of cases of subclinical hypothyroidism has grown substantially in recent years. Unfortunately, the standard treatment protocol for subclinical hypothyroidism, in most cases, is still the same as that for clinical hypothyroidism and involves synthetic thyroid hormone substitution such as synthroid (levothyroxine sodium). This type of treatment has become controversial, and a meta-analysis by the Cochrane Collaboration has shown no benefit and substantial risk in taking synthetic thyroid medication for subclinical hypothryoidism. The risks include the possibility of stimulating hyperthyroidism as well as increased cardiovascular risks from the medication. This type of standard treatment does not address the many factors that cause of contribute to the thyroid dysfunction, and is inappropriate treatment for the high percentage of cases that present as subclinical hypothyroidism.

Fortunately, use of bio-identical hormone therapy and Complementary Medicine is finally being used with great success, even among a small percentage of M.D.s, over the objection of the big pharmaceuticals. Studies have proven that use of T3 and dessicated thyroid in the treatment may control the deficiency of thuroid production with fewer risks and side effects. One study showed substantial benefit from T3 use for both mood and cognitive ability, while a study of dessicated thyroid showed benefits across the board in symptom improvement compared to standard synthetic T4 use. This type of natural thyroid extract, called Armor Thyroid, was used successfully for decades in standard medicine without significant problems, but was all but eliminate from standard practice when patentable synthetic thyroid hormones were developed. Integrating a variety of treatments of Complementary Medicine into the treatment regimen is now proven to benefit the patient in a number of ways. Use of iodine/iodide supplement, selenium, and other nutrient medicines have been proven useful in therapy in numerous studies. The use of chelating agents and detoxification with herbal medicine, supported with acupuncture therapy to stimulate improved physiological reaction, may also be useful for a high percentage of patients. Each year the research uncovers more and more roles for Complementary Medicine to address the variety of factors involved in these diseases, and a knowledgeable TCM practitioner may take advantage of this research and tailor a comprehensive treatment protocol for each individual.

Treatment protocols with hypothyroid conditions require accurate diagnosis and monitoring. Active hormone panels via saliva and blood spot tests have gained much renown in recent years for their accuracy and are relatively inexpensive. Since the patient gathers the samples, the tests can be performed outside of the hospital setting, which is ideal for the acupuncture TCM care. Patient levels of TSH, free T3, free T4, thyroid peroxidase antibody, cortisol, androgens, estradiol, progesterone, vitamin D3, DHEA-S and fasting insulin may be monitored this way. The thyroid profile of TSH, fT3, fT4 and TPO may cost as little as $240, and will usually be covered by your health plan. If the levels indicate clinical hypothyroid condition, the TCM physician will refer you to an endocrinologist to insure proper care in the complementary setting. If the case is subclinical, acupuncture and a variety of herbs and nutritional substances have been shown to be very effective when prescribed intelligently.

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, fatique, sensitivity to cold, metabolic disorder, constipation, and other signs of slow metabolism often have occured 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.

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. 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 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. Deficient active Vitamin D3 may also inhibit the T3 receptors, and supplementation with cholecalciferol may be warranted.

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 fo alpha-lipoic acid. We see from this extensive list why this condition is becoming more prevalent in our population.

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

Since hypothyroidism and hyperparathyroidism is often associated with hypothalamic dyfunction or deficiency, hormonal imbalances are frequently seen. Problems with normal secretion of luetinizing and follicle stimulating hormones, 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, including most anti-depressives and anti-anxiety agents, many hypertensive drugs, some stomach acid controlling medications, and the pain reliever Flexeril, 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.

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.

Treatment Protocol in Hypothyroid and Hyperparathyroid Syndromes with Complementary Medicine

As stated, the treatment protocol in these disorders are complex and individually tailored to the individual health problems that contribute, or to health problems that are caused by the syndromes. The patient needs to take a proactive approach and find a knowledgeable physician to work with. Nevertheless, here are a few approaches commonly included in therapy, to be used as an example of the type of comprehensive therapeutic approach that may be needed. As stated, monitoring of thyroid hormones, along with steroid hormones and Vitamin D3 metabolites, is highly recommended in subclinical hypothyroid conditions, and there is much potential with bioidentical thyroid hormone therapy when necessay. An increasing number of M.D.s are adopting a more comprehensive and holistic approach and working within an Integrative medical model, so the patient may seek out a therapeutic team in Complementary Medicine that now utilizes both an M.D. specialist as well as a TCM physician, or Licensed Acupuncturist.

The question of utilizing synthetic thyroid hormone in the treatment of sublclinical hypothyroidism has long been a subject of hot debate. Most medical specialists have been discouraging of this treatment option for decades, for fear of negative effects on bone mineral density (osteoporosis), as well as the many side effects of therapy affecting a small percentage of study participants. Clinically, the complaints of patients on chronic synthetic thyroid medicines have also discouraged the start of this treatment for subclinical hypothyroid cases. The risks did not outweigh the benefits in the minds of most specialists. Recently, small studies have been created to dispel this notion, and some reviews have found that synthetic thyroid hormone has no significant effect on bone mineral density. The authors caution that the size, nature, and quality of these studies indicate that this is still a preliminary conclusion, and there is need for further studies which review more parameters of bone health than bone mineral density, as there is an increased incidence of bone fractures with chronic use of synthetic thyroid hormones. As usual, the focus on a single risk factor has diverted the question of risk versus benefit away from overall quality of life considerations and the array or negative effects. The bottom line for many patients and medical specialists is now the choice between restoring overall health to correct the problem, or choosing to take a single pill, and ignoring overall hormonal health. All of this diverts the patients and physicians from the most logical conclusion, that whether or not the patient choosed to utilize synthetic thyroid medications, there is still a need to address overall hormonal health with Complementary Medicine and holistic therapy. The patient centered approach educates the patient, allows them to make the choice, and then provides the integrative care needed to restore a healthy state no matter what the choice is.

Another concern raised by a number of medical organizations devoted to endocrine pathology and thyroid issues is the large percentage of cases of subclinical hyperthyroidism that result from chronic use of synthetic thyroid hormone. The demand for thyroid hormone in the patient with hypothyroidism may be variable, and requires consistent monitoring and adjustment of dosage. If the dosage becomes too high, the reaction of the body is to bring TSH levels to a very low level. This very low TSH secretion, controlled by the hypothalamus, is the determining diagnostic factor in subclinical hyperthyroidism, and has an impact on overall health. Symptoms such as tiredness, nervousness, agitation, tremors of the hands or face, heart palpitations, shortness of breath, unusual sweating or intlerance to heat, and weight loss are seen in hyperthyroid states. The most prevalent cause of subclinical hyperthyroidism is chronic use of synthetic thyroid hormome medication, with other drug causes and nodular goiter also associated with a large percentage of cases. While these symptoms may onset slowly and gradually, and not present alarming intensity, subclinical hyperthyroidism does negatively affect quality of life and is associated with a much higher incidence of tachycardia and atrial fibrillation, as well as osteoporosis. This has led many medical doctors to question the chronic use of synthetic thyroid medication, and explore utilization of Complementary Medicine to help restore the thyroid function without drugs when possible.

In combination hyperparathyroid and hypothyroid syndromes, a holistic approach to health is highly recommended as well, and individualized analysis and treatment should be utilized. Gastrointestinal dysfunction and intestinal immune hyperreactivity, such as Celiac disease, is often seen, and should be addressed to aid the various mechanisms of calcium and phosphate regulation, and to take stress off of the body. Stomach dysfunction may have a direct effect on thyroid function as the gastric hormones have a direct effect on levels of the thyroid hormone calcitonin. Adrenal deficiency and overall hormonal balance and homeostasis needs to be addressed and corrected. Dehydration often accompanies hypercalcemia in parathyroidism, and sufficient hdyration and improved kidney adrenal function are needed to correct this problem.

D3 hormone metabolism needs to be normalized. As stated, we still stubbornly call this molecule Vitamin D despite the knowledge that it is a hormone. The best form of D3 is cholecalciferol, which is a prohormone. We cannot treat this supplement lightly, as if it is like Vitamin C. It is a prohormone, and monitoring as well as restoration of hormonal balance should be considered. Restoration of D3 involves healthy cholesterols, sun exposure to the skin, healthy liver function and healthy kidney function. Sometimes, supplementation with cholecalciferol, either normal dose or temporary high dose, may be helpful. Hormone and D3 levels may be monitored with active metabolite testing. Excess circulating D3, called Vitamin D intoxication, has been seen as a cause of hypercalcemia, although most cases involve lesions or tumors in the kidney or adrenals, and not excess supplementation with the prohormone.

Calcium supplementation may be used in some cases as therapy, but the patient should note that calcium is the most highly regulated molecule in the body, and we should quit acting like this mineral can be taken like Vitamin C as well. High dose Calcium carbonate has been found to be successful in cases of hyperparathyroid dysfunction, but only in high dose, and using quality calcium supplement. This type of therapy needs to be monitored, as circulating calcium and phosphate excess may occur, resulting in calcium deposition in tissue that leads to arthritis, soft tissue pain and injury, urinary stones, and calcification of organ tissue. Long-term calcium supplementation with poor quality or the wrong type of calcium molecule may be detrimental to the patient. One useful form of calcium in hypothyroid conditions is calcium pantothenate, a form of Vitamin B5, sometimes called pantothenic acid. If osteoporosis or weak bones are a consideration, calcium hydoxyapatite in a formula designed to increase absorption capability is desirable. A knowledgeable professional should be consulted to determine the need for and type of calcium supplementation that is useful to the individual condition.

Inflammatory stress needs to be decreased in many cases of thyroid dysfunction. Restoring healthy muscle and joint tissues, taking herbs and antioxidants, as well as proteolytic enzymes, may be helpful. In some cases, immune stimulation and restoration of healthy immune function is needed. Hypothalamic function needs to be restored in most cases. Some supplements that help restore hypothalamic function are CaAEP (calcium AEP), P5P (active Vitamin B6), B12 sublingual, pantothenic acid, maca, and inositol hexacotinate B3. DIM and vitex are also helpful. Acupuncture has been proven to have significant effects on hypothalamic function, and scientific studies are cited below. Thyroid function needs to be restored. This may involve monitored use of natural iodine, as well as restoration of adrenal function, and could involve correcting inflammatory problems as well as metabolic problems at the thyroid receptors. Some supplements useful in the protocol are zinc methionine, selenium, L-tyrosine, and B2, and a variety of herbs and formulas can be utilized, including those with extract of dessicated adrenal cortex, and PKA. Tinctures with Ashwagandha and Red Clover may also be utilized. Many of these therapies need to be monitored by a professional. Immune functions should be restored to as healthy a state as possible. While this is a long list, not every patient will need all of this therapy, and a step-by-step approach is important. Gradual restoration and cure should be expected.

If there is a problem with conversion of thyroid hormone in peripheral tissues, the list of possible causes and contributors needs to be examined, and the patient should be treated with appropriate supplementation, decrease in medication where possible, changes in diet and lifestyle as appropriate, and holistic therapy. Hormonal imbalances such as adrenal stress and dysfunction with altered diurnal cortisol could be involved. A lot of this treatment protocol should be the responsiblity of the patient, as the physician has only so much capacity to monitor these various aspects of the problem. The patient needs to take a proactive approach and insure that the various problems are addressed in and intelligent manner, step by step, but needs a knowledgeable physician to explain and monitor the progress with nutrient supplements and dietary and lifestyle changes as appropriate.

Iodine supplementation is often useful in thyroid dysfunction. Iodine is used by the thyroid gland to form circulating thyroid hormone, and the removal of the iodine allows the thyroid hormone to function at the peripheral tissue receptors. This process is controlled in part by thyroid peroxidase enzyme. In autoimmune thyroiditis, commonly called Hashimoto's, antibodies form to attack the thyroid peroxidase. Since iodine is essential to thyroid hormone function, supplementation with iodine may help restore thyroid function, especially if the patient is deficient in iodine. The use of iodine as a supplement was well studied in the nineteenth century, and the safest and most effective form, called Lugol's solution was first made in 1829, and is a combination of elemental iodine with potassium iodide. Lugol's solution was the most popular medicinal supplement in the early twenthieth century, and many people used Dr. Lugol's solution, with almost no evidence of side effect, or ill effect. Today, this same solution is used as a supplement in the form of Iodoral, available in a moderate dosage of 12.5 mg, or in a larger dosage of 50 mg, both of which contain less elemental iodine than Lugol's solution. Iodine levels may be tested with a urine collection test. A small percentage of patients with autoimmune thyroiditis will have a genetic propensity to overstimulate the thyroid with a larger dosage of iodine, and so monitoring by a physician is necessary for safety. Studies have revealed, though, that if symptoms of hyperthyroidism are noted, that these are reversed quickly by reducing or stopping the iodine supplementation. Since iodine stores in the tissues, supplementation may be needed for a few months to replenish the iodine stores.

Besides being important to the formation of active thyroid hormone, iodine also serves as an important antioxidant in the body, and is protective against cancerous mutation. The highest concentrations of iodine are in the thyroid gland and the breast tissue, and so sufficient iodine is protective against breast cancer. Lugol's solution has also been widely used to block the effects of radiation in the form of radioactive iodine, and was widely distributed after the Chernobyl accident. Moderate iodine supplementation has been shown to modulate the genetic expression of thyroid stimulating hormone receptors to prevent Hashimoto's thyroid dysfunction (see the study citation below), and is proven in a number of studies to normalize various aspects of the thyroid metabolism in hypothyroidism. Lugol's solution has been used, with monitoring, to treat hyperthyroidism by inhibiting the organification of iodine in the thyroid gland. Iodine deficiency, in many geographical areas of the United States, has been found in a large percentage of targeted population, especially in women over 40 years old. The resurgence of prescription and general use of Lugol's solution, which has always been available over the counter, has been a concern of the pharmaceutical industry, which makes much profit from the sales of synthetic thyroid hormone. Restriction of the purchase of Lugol's solution was initiated in 2007 in the United States, purportedly to prevent its use in the making of methamphetamines, although the evidence of this use is scant.

As stated, the Complementary Medicine physician, such as the knowledgeable Licensed Acupuncturist and herbalist, may treat a variety of conditions associated with hypothyroid states as well as the condition itself. Cardiovascular health, immune health, neurological health, metabolic health, and side effects of radiation and chemotherapy, are just some of the aspects to this overall condition that may be addressed with Compelemtary Medicine. There are so many reasons to incorporate Integrative Medicine into your care that they can't be properly addressed in this web article. The time, expense and effort you invest in this type of care will pay great dividends to your overal health and productivity.

Information Resources

• Wikipedia gives a clear explanation of hypthyroidism. Most standard medical websites provide an incomplete explanation for patients that suspect a subclinical thyroid imbalance, or have been diagnosed with either sublclinical or clinical hypothyroidism. In this disease, or health imbalance, patient understanding is the key to correcting the endocrine imbalance and the associated health problems. Goto http://en.wikipedia.org/wiki/Hypothyroidism
• A 1995 landmark study entitled the Colorado thyroid disease prevalence study indicated that abnormally high levels of TSH exists in about 10 percent of the population, and abnormally high levels of TSH exists in over 2 percent. The study also noted that among patients in a large cross-sectional study of 25,862 persons attending health fairs, that over 40 percent that were taking thyroid medications still had abnormal TSH levels. One measure of associated health problems was conducted, lipid imbalance, and this was highly correlated with abnormal TSH levels. The results of this large study indicate that nearly 13 percent of a normal midwestern population may have a subclinical thyroid disorder or a poorly treated clinical disorder. The time to integrate Compelementary Medicine into the treatment protocol and take a holistic approach to restoration of health has come, yet standard medicine still is resisting this logical and conservative approach to treatment.http://www.ncbi.nlm.nih.gov/pubmed/10695693
• A broad study of the general population in France in 2004 found that among patients not already diagnosed with thyroid disease that the prevalence of abnormal TSH was very high, indicating an alarming percentage of the population in industrialized society now experiencing a subclinical thyroid imbalance, with a significant percentage associated with deficient iodine levels and other environmental factors. Undiagnosed subclinical hypothyroidism in the female population age 45-60 was over 11 percent. http://www.ncbi.nlm.nih.gov/pubmed/15731735
• Dr. John R. Lee, a pioneer in the use of bio-identical hormones, is well represented with hypothyroid information at http://virginiahopkinstestkits.com/thyroidarticle.html
• A 2006 study at the University of Gottingen Medical School in Germany found that common environmental chemicals used in sunscreen are accumulating in our drinking water and causing potential hormonal imbalances similar to hypothyroidism: http://www.endocrine-abstracts.org/ea/0011/ea0011oc60.htm
• A 1999 meta-analysis of published scientific studies by the University of California Neuropsychiatric Institute in Los Angeles found that the drug Lithium, used to treat depression and bipolar disorders, interfered with thyroid metabolism and increases the incidence of both overt and subclinical hypothyroidism, and that subclinical hypothyroidism is associated with neuropsychiatric symptoms. Lithium is now available without prescription and will be heavily promoted for profit: http://www.ncbi.nlm.nih.gov/pubmed/10221287
• A 2005 study of the effects of hypothyroidism found that when thyroid hormone in circulation (thyroxine or T4) was reduced, this created a deficiency of the important cellular antioxidant and detoxifier, glutathione, in the red blood cells, which would increase cardiovascular risk, risk of anemia, and risk of leukemia: http://www.ncbi.nlm.nih.gov/pubmed/15801865
• A 2008 study at the Norwegian University of Science and Technology found that there was a 40% increased risk of cardiovascular death over 8.3 years with women who had a high TSH (thyrotropin) level, but not with men. The connection was not clear, and the authors did not advocate treating with synthetic thyroid hormone, but did suggest that thyroid health and general health should be addressed in these conditions: http://www.theheart.org/article/860257.do
• A 1992 study investigating the relationship of hyperparathyroidism and hypothyroidism found that 95% of laboratory animals with induced high levels of TSH developed hyperparathyroid state in 12 weeks: http://www3.interscience.wiley.com/
• Scientific study in China in 1997 has proven that acupuncture exerts significant beneficial effects on the hypothalamus: http://www.wellspringintegrative.com/acup_pit.htm
• A 2006 review of parathyroidectomy versuse partial removal and minimally invasive techniques showed that outcomes were similar, with calcium and parathyroid hormone levels normalizing at 3 months (Rush University Medical Center, Chicago): http://www.sciencedirect.com/
• A study of the long-term effects of synthetic thyroid medication, levothyroxine, in 2008 at the University Federico II Dept. of Intenal Medicine and Cardiovascular Sciences, shows association with impaired heart function and arterial hardening that explains complaints of fatique: http://www.ncbi.nlm.nih.gov/pubmed/18445676
• Reports of long-term side effects of synthetic thyroid medication to the FDA: http://www.ehealthme.com/q/levothyroxine+sodium-side-effects
• Inflammatory mediators such as interleukin-6 have been found to play an important role in the pathogenesis of hypothyroidism, and immune dysfunction as well as physiological stress and hormonal imbalance increase the chance that chronic inflammation will play a part in the disease: http://www.annals.org/content/128/2/127.abstract
• A 2010 study at Istanbul University in Turkey found a significant correlation between diabetes, autoimmune thyroid disease and celiac disease, with 15.4% of children with insulin dependent diabetes (an autoimmune disorder), also testing positive for the antibodies that confirm Hashimoto's thyroiditis: http://www.ncbi.nlm.nih.gov/pubmed/20931425
• A 2009 study at Boston University Medical Center found that a number of common environmental pollutants, including PCBs, PBDEs, perchlorates, bisphenol-A in soft plastics, pesticides and dioxins, may cause of contibute to thyroid dysfunction in a variety of biochemical ways: http://www.ncbi.nlm.nih.gov/pubmed/19942155
• A high percentage of the U.S. population in areas of the country have been found to be iodine deficient, and iodine has been a safe and broadly prescribed treatment for various hypothyroid conditions for more than a century. The benefits revealed in scientific studies are broad, and this 2010 study at Leipzig University in Germany reveals that iodine supplementation may prevent peripheral thyroid dysfunction, mutations of the thyroid stimulating hormone receptor, and slow the development of clinicially relevant thyroid diseases, including Hashimoto's thyroiditis, an autoimmune disorder:http://www.ncbi.nlm.nih.gov/pubmed/21035537
• To see the effects of fluoride consumption, a halogen that competes with iodine absorption, along with bromides, and may limit iodine in the body, refer to this website of the fluoride action network:http://www.fluoridealert.org/health/
• Research as far back as 1997, at the University of Brussels, in Belgium, showed in animal studies that a moderate dose of iodine/iodide supplement normalized thyroid hormone production, thyroid stimulating hormone (TSH) level, and thyroperoxidase (TPO), which is the enzyme needed to control the rate of transfer of iodine to form thyroid hormone in the gland. The findings showed that a small dose, as is commonly seen in many supplements these days, had no effect: http://www.ncbi.nlm.nih.gov/pubmed/9296378
• Research in 2005 at Cardiff University School of Medicine in Great Britain found that sufficient iodide levels in the body inhibit the mutations of thyroid stimulating hormone receptors (TSHR), which are the main mechanism of pathology in Hashimoto's thyroiditis, and in adenomas and multi-nodular goiter. Thus, periodic supplementation with Iodoral, when warranted, may prevent these diseases from occurrring: http://www.ncbi.nlm.nih.gov/pubmed/15691889
• A 2010 metaanalysis of scientific studies of selenium supplementation in cases of Hashimoto's thyroiditis found that patients supplementing for 3 months had significantly lowered thyroid peroxidase antibodies (TPOab) and significant improvement in symptoms: http://www.ncbi.nlm.nih.gov/pubmed/20883174

NOTE: medical experts have stated for many years: “long-term use of high-dose inhaled corticosteroid therapy has potential to cause systemic side effects – impaired growth in children, decreased bone mineral density, skin thinning and bruising, and cataracts. Hypothalamic-pituitiary-adrenal-axis suppression, measured by serum or urine cortisol decrease correlates with the occurrence of systemic side effects of high-dose inhaled corticosteroids.”

The information on this website is not intended to be used as a specific medical advice or cure. Please consult with the practitioner or an appropriate physician, such as a licensed acupuncturist, naturopath, or medical doctor, to discuss the proper application of the information contained on this website.