(Underactive Thyroid)

ARTICLE #1 The Thyroid Gland and Its Hormones

ARTICLE #2 Signs of Thyroid Function (DeGowin)

ARTICLE #3 Thyroid Blood Tests

ARTICLE #4 Causes of Hypothyroidism

ARTICLE #5 Estrogen Dominance and Hypothyroidism

ARTICLE #6 Natural Treatment for Hypothyroidism

ARTICLE #7 Lugol's Solution

ARTICLE #8 Iodine in the Body (coming soon)

ARTICLE #9 Environment and the Thyroid (coming soon)

The Thyroid Gland and Its Hormones

The Greek word for "thyroid" means "shield-shaped". It consists of two lateral lobes whose upper halves lie on either side of the projecting thyroid cartilage (Adam's apple). The lower halves of the gland are at the sides of the trachea. The normal adult thyroid is usually not palpable. In a thin neck, the normal isthmus may be felt as a band of tissue that just covers the surface outlines of the tracheal rings. A goiter is any enlarged thyroid gland, regardless of the cause, that may palpated or even visibly seen.

The principal function of the thyroid gland is to synthesize and secrete the thyroid hormones necessary for normal metabolic processes. The production of thyroid hormones is influenced by intricate regulatory mechanisms and may be altered by many physiologic, pathologic, and drug related factors. The thyroid glandalso produces calcitonin, which is not of concern in this article.

The thyroid gland secretes two hormones which are derived from the amino acid tyrosine and the incorporation of dietary iodine. The major secretory product of the thyroid gland is T4 (thyroxine) which contains four iodide atoms. The other product is T3 which contains three iodide atoms. The T3 is secreted in small amounts, but is the most active form of thyroid hormone.

The synthesis of thyroid hormone occurs at the interface of the thyroid cell and the colloid. Within the thyroid follicle, the iodine is oxidized. This activated form of iodine attaches to the amino acid tyrosine, forming either a monoiodotyrosine (meaning 1 iodine and 1 tyrosine) or a diiodotyrsonine (meaning 2 iodines and 1 tyrosine). These iodotyrosines then combine with each other in a reaction that forms either T3 or T4. If a monoiodotyrosine and a diiodotyrosine combine (1 plus 2), the result is triiodotyrosine ( 3 iodines and 1 tyrosine = T3). If the union of two diiodotyrosines (2 plus 2) occurs then the result is tetraiodotyrosine (4 iodines and 1 tyrosine = T4). These newly formed thyroid hormones are then stored in a glycoprotein called thyroglobulin. The thyroid hormones then remained stored until its release is intiated by TSH (Thyroid Stimulating Hormone), which comes from the pituitary gland.

Once the thyroid is told to release its hormones T4 and minute amounts of T3 enter the circulation. Once these hormones are released into the circulation they are bound to thyroid-binding globulin (TBG -85%), albumin (10%), and transthyretin (prealbumin - 15%). These binding proteins allow the thyroid hormones to remain soluble in plasma where they are able to be delivered throughout the body. Not all T4 and T3 is bound to TBG. A limited amount of thyroid hormone circulates freely in the plasma in metabolically active forms called freeT4 and freeT3.

Under normal circumstances, only about 20% of T3 (the most active form) is secreted directly from the thyroid gland. Therefore, the T4 that is bound to TBG must be converted into T3 to become more active. This step is important because of the nutritional cofactors involved, namely selenium, zinc, and copper. Most of the T3 present in plasma is derived from the peripheral conversion of T4 by monodeiodination (meaning, 1 iodine is removed). This process is done by the enzymes called deiodinases (their names aren't important)(these are the enzymes that require selenium, zinc, and copper). This removal of iodine is done in the liver, muscles, kidneys, and anterior pituitary gland.

Control of the release of thyroid hormones from the thyroid gland is done through the hypothalamic-hypophysial-thyroid axis. A fancy way to say from the hypothalamus, to the pituitary gland, to the thyroid gland (in that order). The hypothalamus releases TRH (thyroid releasing hormone). The pituitary gland releases TSH (thyroid stimulating hormone). And the thyroid gland releases T4 and T3. TSH, the glycoprotein secreted by the pituitary gland, regulates not only the release of thyroid hormone, but also iodine trapping and T4 and T3 synthesis within the thyroid gland. The release of TSH from the pituitary is controlled by TRH, a peptide produced by the hypothalamus which is transport to the pituitary by way of the porto-venous circulation. T3 and T4 inhibit the action of TRH on the pituitary gland, thus decreasing the secretion of TSH. The T3 is thought to play a greater role than T4 in inhibiting TSH secretion because the pituitary gland readily converts T4 to T3. The amount of available iodine also influences the intrathyroidal regulation of thyroid hormone secretion. Large amounts of ingested iodine may decrease iodine trapping and hence hormone synthesis and release causing decreases in serum T4 and T3 concentrations and an increase in TSH secretion. When there is iodine shortage or deprivation, and increase of iodine trapping occurs. This feedback is how the thyroid can maintain a constant pool.

The effects of thyroid hormone at the cellular level depends on the binding of T3 to its specific intracellular receptor. Free thyroid hormone crosses the cell membrane by diffusion. After it makes it into the cell it binds to a binding protein and migrates to the membrane of the nucleus where it enters to exert its effects on DNA. There, T3 binds to a nuclear receptor, which in turn regulates transcription, translation, and protein synthesis.

The physiological effects of thyroid hormone include bone growth, CNS (Central Nervous System) maturation, Beta adrenergic effects, increased basal metabolic rate (via increased Na+/K+ ATPase activity= icreased O2 consumption leading to increased body temp), increased glycogenolysis (release of energy stores), gluconeogenesis (formation of new glucose for energy), lypolisis (breakdown of fat for energy), increased cardiovascular effects, and is important for normal lactation.

The metabolic effects of thyroid hormone are also important. Thyroid hormone controls carbohydrate metabolism. In physiologic amounts, thyroid hormone potentiates that action of insulin and promotes glycogenesis and glucose utilization. In pharmacological amounts, thyroid hormone is a hyperglycemic agent.

Protein metabolism is also effected by the thyroid. In physiologic amounts, thyroid hormone has a potent protein anabolic (building) effect. In large doses it has a protein catabolic (break-down) effect.

Concerning fat metabolism, thyroid hormone stimulates all aspects of lipid metabolism. There is a general inverse relationship between thyroid hormone levels and plasma lipids. Elevated thyroid hormone levels are associated with decreases in blood triglycerides, phospholipids, and cholesterol. Decreased thyroid levels show an increase in these substances, especially cholesterol.

In vitamin metabolism the thyroid controls the metabolism of fat-soluble vitamins (A, E, D, and K). For example, thyroid hormone is required for the synthesis of vitamin A from carotene and the conversion of vitamin A to retinene. In hypothyroid states, the serum carotene is elevated and the skin becomes yellow. This skin condition differs from that observed in jaundice in that the sclera fo the eye is not yellow.

Given the above information, one can conclude that the thyroid is involved in many intricate systems of the body. An imbalance in any part of the system can lead to cascading effects throughout the body. In extreme cases of thyroid disfuction one can develop a goiter. A goiter is any enlargement of the thyroid gland regardless of cause. It can be seen in hyper and well as hypothyroidism.

back to top

Signs of Thyroid Function (DeGowin)

(the following may not include subclinical descriptions)

Once the physician has assessed the gross pathologic changes in the thyroid, mostly by inspection and palpation, he turns to the evaluation of the thyroid function by seeking symptoms and signs of two clinical entities myxedema and thyrotoxicosis. The evidence is conclusive that myxedema is purely a deficit of thyroid hormone; hence hypothyroidism is an accurate equivalent expression. But, thyrotoxicosis or Graves disease is not necessarily synonymous with hyperthyroidism, because some clinical features have never been reported in animals or humans. Many ocular phenomena remain unexplained by the present knowledge of the thyropituitary axis. With this reservation, we prefer to tabulate the signs of the two diseases as opposite extremes of thyroid function, to assist your memory.


In thyrotoxicosis the face is think, the features sharp, the expression alert and vivacious; movements of the facial and neck muscles are frequent and fast. The responses to questions are quick; the emotions are labile. In contrast, the face of myxedematous patients are rounded, relaxed, indefinably puffy without frank edema. The expression is placid and goodnatured. Responses are slow.


The voice is normal in thyrotoxicosis. In myxedema its quality is frequently hoarse and coarse, from edema of the vocal cords. The singer can no longer sing; her friends are solicitous because of her "cold" sound.


Spontaneous Movement - In thyrotoxicosis the movements are excessive, and their speed faster than normal. Speech cadence is accelerated; the tongue and wrists can be flipped in alternating motion faster than normal. In myxedema there is paucity of unnecessary motion; the motions are slow and deliberate. The speech is slow and distinct. The alternate motion rate of flipping tongue and wrists is slow.

Muscle Strength - In thyrotoxicosis there is some generalized muscle weakness but symmetric groups seem particularly involved. The quadriceps femoris is most often affected, so the patient must push with arms on the chair or his thighs to arise from a sitting position. Both shoulder girdles may be weak; symmetric pairs of eye muscles may be paralyzed. In myxedema, there is some generalized weakness, but focal atrophy or disability is lacking.

Tendon Reflexes - The reflexes in thyrotoxicosis are normal or hyperactive. In a patient with myxedema, when a knee jerk is elicited, one can see and feel the slow relaxing of muscles after the jerk.

Tremor - Almost always in thyrotoxicosis the extended fingers and tongue exhibit a fine tremor. In addition, there may be a coarse tremor in a group of muscles in the calf or thigh as a result of weakness. The patient with myxedema has no opposite sign.

Tongue - The tongue is normal in thyrotoxicosis; in some myxedema patients the tongue seems large and awkward.


Changes in this tissue are more easily perceived in women than in men.

Skin - In thyrotoxicosis the skin feels softer than normal; it is thin, moist and sweating. The skin over the skins may be the site of circumscribed elevated areas that are firm, nontender, and pink. Paradoxically, this is called pretibial myxedema, although it usually occurs in thyrotoxicosis in association with the exophthalmic syndrome. A counterpart of pretibial myxedema is thickening of the skin on the dorsa of the great toes. In myxedema the skin feels cold, dry, and thick; often there is scaling that is difficult to distinguish from ichthyosis. The palms and circumoral skin may be yellow from carotenemia.

Hair - In thyrotoxicosis the hair on the head is fine in texture, oily, and abundant. In myxedema the hair on the head is dry and coarse, so they emit a crackling sound when lightly brushed. The texture is approached by that resulting from the so-called permanent wave. Looking at the profile of the forearm, one sees paucity or absence of lanugo hairs; or a few lonesome broken shafts may remain. The lateral third fo the eyebrows are often thinned.

The Nails - In thyrotoxicosis the fingernails may separate from its matrix; usually only one or two pairs of nails involved. In myxedema the nails are dry and brittle; sometimes they are longitudinally ridged.


In about one fifth of the patients with thyrotoxicosis, various signs of the endocrine eye lesion may develop, usually after the onset of hypermetabolism. The signs may be lid lag, lid spasm, lacrimation (tearing), chemosis (excessive edema of the ocular conjunctiva), periorbital edema (puffy eyes), and exophthalmos (eyes seem to be sticking out). In myxedema the only ocular sign is periorbital edema.


Strength of Contraction - In thyrotoxicosis the strength of myocardial contraction is augmented, as manifest by the accentuated precordial thrust and the sharpness of the heart sounds. In myxedema the precordial thrust is normal or feeble.

Cardiac Rate - Tachycardia (rapid heart rate) is almost the rule in thyrotoxicosis. In myxedema the ventricular rate is normal or slow.

Cardiac Rhythm - Thyrotoxicosis in notorious for the high incidence of atrial fibrillation and atrial flutter. In myxedema, dysrhythmias are rare.

Blood Pressure - In thyrotoxicosis the systolic pressure is slightly elevated, the diastolic diminished, so the pulse pressure is widened; thus a pistol-shot sound is often present in the femoral arteries. In myxedema the blood pressure is normal, or else there is moderate elevation of both systolic and diastolic values that may return to normal with treatment.


Food Intake - The caloric intake is frequently increased in thyrotoxicosis, usually with contrasting weight loss; the weight depends on whether the patient can take enough food to meet the increased caloric requirements. In myxedema food intake may be small with constant or gaining weight.

Intestinal Motility - In thyrotoxicosis defecation may be more frequent; the onset of true diarrhea is a grave prognostic sign. Constipation is very common in myxedema; the resulting tympanites (distention of the abdomen, due to the presence of gas or air in the intestine) may suggest ileus (obstruction of the intestines).


In thyrotoxicosis body fluid does not accumulate unless cardiac failure occurs. In advanced myxedema pericardial effusion, ascites, and edema of the ankles can all occur without cardiac failure.


In thyrotoxicosis the menses are usually normal; occasionally there is oligomenorrhea (menstrual flow less than normal). In myxedema, menorrhagia (excessive menstrual flow) is common.


The erythrocytes are usually normal in thyrotoxicosis, but leukopenia sometimes occurs. In myxedema a normocytic or macrocytic anemia is frequent. The anemia is refractory to therapy with iron, vitamin B12, or anything else but thyroid hormone. Platelets are dysfunctional.


(The human faculty for thought, judgment, and emotion.)

Mentation - In thyrotoxicosis there is no disturbance. The patient with myxedema often complains of thinking more slowly; this can readily be confirmed by objective measurements.

Emotional Affect - Patients with thyrotoxicosis are notoriously irritable and emotionally labile. Most patients with long-standing myxedema appear cheerful and placid; but those with recently acquired symptoms complain bitterly and are often dejected.

Psycoses - Depressions are common in thyrotoxicosis; occasionally manic states develop. Patients with myxedema may develop depressions, though not so commonly as with thyrotoxicosis.

back to top

Thyroid Blood Tests

Most conventional physicians use the following test to detect thyroid problems: TSH Immunoassay, Free Thyroxine Immunoassay (FT4), T4 Immunoassay, Resin T3 (or T4) Uptake, Free Thyroxine Index (FTI), T3, and Free T3. More tests exist for thyroid disorders, but for the purpose of this page we will focus on those related to hypothyroidism.

Without going into details about each test, the reader should already have knowledge of what each test is attempting to find. After reading The Thyroid Gland and Its Hormones each test will make sense from a functional standpoint.

Most physicians use TSH testing as a screening test. They determine the nature of the disorder by the results. For hypothyroidism, physicians use Serum TSH to show either primary or secondary hypothyroidism. TSH will be high in primary hypothyroidism and low in secondary hypothyroidism.

The problem in the real world is that these tests mean nothing.

In the April 19, 1997 issue of the British Medical Journal, Dr. A P Weetman, professor of medicine, wrote:

". . . even within the reference range of around 0.5-4.5 mU/l, a high thyroid stimulating hormone concentration (>2 mU/l) was associated with an increased risk of future hypothyroidism. The simplest explanation is that thyroid disease is so common that many people predisposed to thyroid failure are included in a laboratory's reference population, which raises the question whether thyroxine replacement is adequate in patients with thyroid stimulating hormone levels above 2 mU/l."

In response to Dr. Weetman, David Derry M.D., Ph.D., a thyroid expert and researcher, based in Victoria, British Columbia, responded, saying:

"Why are we following a test which has no correlation with clinical presentation? The thyroidologists by consensus have decided that this test is the most useful for following treatment when in fact it is unrelated to how the patient feels. The consequences of this have been horrendous. Six years after their consensus decision Chronic fatigue and Fibromyalgia appeared. These are both hypothyroid conditions. But because their TSH was normal they have not been treated. The TSH needs to be scrapped and medical students taught again how to clinically recognize low thyroid conditions."

In an interview with this same Dr. Derry, he stated the following:

"The thyroidologists have been looking for a reliable test for thyroid function since the beginning of the century. The first important ones were the Basal Metabolic Rate, the cholesterol and the creatine phosphokinase (CK) . These were used mainly up to about 1960. If you had a high cholesterol in the first half of the century you got thyroid to lower it to normal. Details of using this method of treatment were still described in the 1950's. The Basal Metabolic rate became the fad in the 30s and 40s and almost every office had a machine to measure it. It was quite good but subject to difficulties of interpretation and interference by emotional factors. However it still remains the only test that actually measures the effects of thyroid medication on the human body. In the 1940's radioactive iodine became available from the Tennessee Valley Atomic Energy Complex. Hence the metabolism of iodine could be studied more closely. The radioactive iodine uptake by the thyroid became a frequently used test, which was said to be infallible like all the others when they first arrived. Every time there was a new test it was declared to be reliable for telling if a person was hyperthyroid or hypothyroid, but as with every previous test it turned out to not be clinically applicable in all cases. In the 1960's when I was studying medicine the PBI (Protein bound iodine) was heralded as the only test necessary, when it was low you had hypothyroidism and when it was high you had hyperthyroidism. This was written in some of the textbooks of the time. Eventually this test went the way of the rest -- useful sometimes-- but doesn't always agree with the clinical findings.

Next came the T4 or total thyroxine in the blood that is the free and the protein bound thyroxine measured together. This was also hailed as far superior to the PBI, but it too went the way of the rest of the tests --as not being reliable enough. Finally the TSH arrived in the late 60s and was boasted about as the final answer. The TSH was not only able to deliver all the thyroid diagnoses but it could be used as well for monitoring therapy. Over the following twenty years the TSH was made more and more sensitive and because of these improvements it was even more thought that it was the total answer for thyroid diagnosis and treatment. However as the TSH was so sensitive to orally-given thyroid hormone it meant literally everyone was going to end up with a low dose by comparison with previous doses. The new doses were about a third of the dose that had been found to be clinically effective for every patient for eighty years prior to the TSH.

The TSH had a ring of scientific rigor for those who have a smattering of knowledge about thyroid metabolism. It was part of the pituitary feed back mechanism for monitoring the output of the thyroid gland. There is no doubt that it does accomplish this job. But unfortunately the TSH value has no clinical correlation except at absolute extremes with the clinical signs or symptoms of the patient. The reasons for this are complex and I only want to discuss one aspect but there are other important factors.

To start with the thyroid metabolism is controlled locally in the tissue by each organ. That is the brain has one mechanism for controlling the amount of thyroid available to the brain but it is different from other tissues such as the liver. There are many mechanisms by which each tissue controls the amount of thyroid hormone which gets into the tissues. But to discuss one: there is an enzyme in the tissue which deiodinates (takes one iodine off the thyroxine T4) and makes T3 or triiodothyronine. These enzymes are called deiodinases. Every tissue has different types of deiodinases. To just give you one example: If you starve animals and study the deiodinases in the brain and liver you find that the activity in of the brain deiodinases go up by 10 times while at the same time the liver deiodinases go down--not up. This mechanism is obviously meant to preserve the functioning of the brain under starvation conditions and not metabolize too much thyroid hormone in the liver. Therefore the control of thyroid metabolism is in every individual tissue. The problem with this is-- if a tissue needs more (such as the brain with depression) there is no way for the brain to signal the thyroid that it needs more sent up to it. The thyroid merrily goes on putting out the same amount of thyroid hormone. So the patient can have symptoms related to low thyroid in the brain (for example) but the thyroid doesn't do anything about it. But if you give thyroid hormones in an adequate dose the brain symptoms will disappear. Meanwhile the other tissues and organs adapt to the increased circulating hormones that you have used to fix the brain with. The adaptation of the tissues to different levels of circulating hormones has been shown in the literature.

The symptoms of low thyroid, which are numerous and variably expressed, can be related to any organ or system in the body and partly depends on the person's genes. But because of the all inclusiveness of the TSH medical students are not taught or only superficially taught the symptoms of low thyroid. The TSH was "scientific" and held all the answers to thyroid disease. If you have not lived through several versions of the ultimate test for thyroid then it is harder to grasp this phenomenon."

Another reason that the tests are often inaccurate is because they only show what your thyroid hormone levels are on the day of testing. Your thyroid is a "tricky" organ to both diagnose and treat since its hormone levels fluctuate all the time. What you eat each day has a tremendous and immediate impact on it, and how much hormone it secretes.

Another reason for their inaccuracy is that the tests do not indicate if your thyroid hormone is really entering your cells. Your thyroid may be manufacturing plenty of hormone but your cells have become resistant to the hormone and are not able to utilize it.

So what should you do if blood tests are not accurate?

Before the use of blood measurements, it was common to diagnose hypothyroidism based on basal body temperature (the temperature of the body at rest) and Achilles reflex time (reflexes are slowed in hypothyroidism). Treating hypothyroidism until symptoms disappear has also been a long proven option for returning the patient to normal.

Basal Temperature Self Test

The basal temperature test is a better index of hypothyroidism and need for thyroid therapy than the basal metabolic rate test. It is done upon waking in the morning while the body is completely at rest, before engaging in any activity or eating anything, before getting out of bed, even to urinate. The thermometer should already have been shaken down the night before so as not to create heat from the muscle activity of shaking the thermometer. The thermometer is placed in the mouth for ten minutes by the clock while resting quietly. Body heat depends upon the amount of foodstuffs burned. Thyroid hormone is essential for the oxidation or burning of fuel in the body, and in the thyroid-deficient person body temperature falls below normal because of inadequate oxidation.

The normal range of basal temperature is between 97.8 and 98.2 degrees Fahrenheit, if there is no sinus or throat infection present. A reading below this normal range suggests low thyroid function. If it is above the normal range, one must be suspicious of some infection or an overactive thyroid gland. In women of menstruating years, because temperature can be elevated with ovulation, basal temperature is best measured on the second and third days of the period after flow starts. Before the menarche or after the menopause, the basal temperature may be taken on any day. When symptoms of thyroid deficiency are present, the basal temperature may be one, two, or even three degrees below normal. With thyroid therapy, the temperature will start to rise toward normal.

Lugol's Solution Skin Test has been another method of testing thyroid function by Naturopathic doctor. For this reason, a separate article has been written and should be referred to thereof.

Cholesterol and Hypothyroidism*

Hypothyroidism is the second leading cause of high cholesterol, after diet. When thyroid hormone levels drop, the liver no longer functions properly and cannot utilize cholesterol properly leading to an excess cholesterol, fatty acids, and triglycerides. With this knowledge, cholesterol levels can be used to detect if the thyroid gland is not working properly. If your regular thyroid test comes out normal (which we now know will most of the time), but you have the symptoms of hypothyroidism and your cholesterol levels are high, then odds are you have hypothyroidism.

back to top

Causes of Hypothyroidism

Hypothyroidism is the underactivity of the thyroid gland. It is a condition which occurs when the thyroid gland fails to produce enough thyroid hormones or it can be a failure of the tissues to utilize thyroid hormones. Some causes are common and some are less common.

Iodine Insufficiency - Millions of individuals develop hypothyroidism due to the lack of adequate iodine intake which is usually due to soil depletion and lack of iodine in our diet. Since iodine is necessary for the synthesis, storage, and secretion of thyroid hormones, this deficiency of iodine leads to hypothyroidism.

Hashimoto's Disease - This is a thyroiditis (inflammation of the thyroid gland) with lymphocitic infiltration and circulating antithyroid antibodies. The thyroid gland is usually diffusely enlarged, firm, and finely nodular. Although patients complain of neck thightness, pain and tenderness are not usually present. Depression and fatigue are common in people with Hashimoto's. About one-third have mild dry mouth or dry eyes. This can cause hyperthyroidism as well as hypothyroidism. It is proposed that a lack of iodine also plays a role in autoimmune attacks on the thyroid.

Radioactive Iodine - Overtreatment of Grave's Disease or Hashimoto's Disease with radioactive iodine causes a high incidence of hypothyroidism several years after the use of radioactive iodine, even when small doses are given. Hypothyroidism also occurs quite frequently years after surgical or medical treatment of Grave's disease.

Thyroidectomy - In thyroid removal surgery, if too much of the thyroid gland is removed, the result can be hypothyroidism.

Pituitary Gland Disorders - Tumors or any other disorder that can cause hypopituitarism can lead to thyroid-stimulating hormone deficiency. Disorders of the hypothalamus may also cause thyroid hormone deficiency. Trauma, such as from automobile accidents, surgery, or postpartum pituitary necrosis (Sheehan's syndrome), could lead to hypopituitarism and result in hypothyroidism.

Drug Induced Hypothyroidism - Certain drugs are known to interfere with the function of the thyroid. These drugs include, but are not limited to: Lithium, iodine, propylthiouracil or methimazole, phenylbutazone, sulfonamides, amiodarone, interferon-alpha, and interleukin-2. Lithium, used in the treatment of bipolar manic-depressive disorder, inhibits thyroid hormone release. Amiodarone causes clinically significant hypothyroidism in about 8% of patients because of its high iodine content (remember that too much iodine can downregulate the function of the thyroid).

Goitrogenic Foods - Goitrogenic foods like brussel sprouts, rutabaga, turnips, kohlrabi, radishes, cauliflower, African cassava, millet, babassu, cabbage, kale, turnips and soy products all can inhibit the function of the thyroid.

Cigarette Smoking - Tobacco smoke contains cyanide, which is converted to thiocyanate, and acts as an anti-thyroid agent, inhibiting iodide uptake and hormone synthesis.

Environmental Exposures - Some patients have experienced the fact that fluoride and chlorine can interfere with proper thyroid conversion and result in hypothyroidism. Another concern is mercury, a component in dental fillings, which can disable the thyroid's ability to convert T4 to T3, resulting in hypothyroidism.

Additional Causes

Polyunsaturated oils interfere with the release and transport of thyroid. Some of these oils include corn oil, soybean, safflower, and sunflower oils.

Estrogen Dominance - see "Estrogen Dominance and Hypothyroidism" article.


Accumulation of Iron in the thyroid gland (10% of those with hemochromatosis)

Adrenal Insufficiency

Thyroid Hormone Resistance

Dysfunction of T4 to T3 conversion (Wilson's syndrome) -There are several conditions that tend to interfere with T4 to T3 conversion. 1) High stress states (or intake of steroids, like prednisone). 2) Chronic illness. 3) Restriction of carbohydrates in the diet. 4) Estrogen. 5) Beta-blockers (used to treat heart disease and hypertension). 6) Hypothyroidism in and of itself. 7) Deficiency of necessary cofactors. For example, the trace mineral selenium is required by the (5' deiodinase) enzyme to convert T4 to T3. Therefore, if a selenium deficiency exists, it follows that T3 production may be impaired.

Congenital Hypothyroidism - being born without a thyroid

Nuclear Plant Exposure

Given the possiblities of causes, one can see how important it is to find the CAUSE of the problem and not to just treat the SYMPTOMS. If you just treat the symptoms, the problems never goes away.

back to top

Estrogen Dominance and Hypothyroidism

One of the most overlooked factors contributing to an under-active thyroid is estrogen dominance. Estrogen replacement therapy and estrogen dominance decreases the function of the thyroid gland. Estrogen partially blocks the efficiency of thyroid hormone. It does so by occupying the thyroid receptor sites.

Estrogen can be potentially dangerous when not counter-balanced by adequate progesterone.

There are many things that can lead to estrogen dominance, some of which are related to our surrounding and the choices we make in our everyday lives. You would have to virtually live in a bubble to escape the excess estrogens you're exposed to through pesticides, plastics, industrial waste products, car exhaust, meat, soaps, as well as much of the carpeting, furniture and paneling that we live with indoors every day.

Too much body fat can lead to estrogen dominance because estrogen is produced secondarily in fat cells. Low-fiber diets can also lead to estrogen dominance because fiber is used to carry estrogen through the bowel for elimination. Excessive amounts of stress can lead to adrenal fatigue, which can also cause hormone imbalances and lead to excess amounts of estrogen in the body.

The liver is a detoxifying organ. If the function of the liver is impaired it can not rid the body of it of harmful chemicals, foods, and excess estrogens.

The aminals that we eat are fed growth hormones and estrogenic hormones to cause rapid growth so they can be put on the market sooner. This is how we end up ingesting a large portion of xeno-estrogens. Sugar and chemical ingestion in processed foods also create chemicals called xeno-estrogens in our bodies, stimulating a vicious cycle in which fat cells are enlarged due to these estrogens, and then fat cells make more estrogen in the body. Young girls, and even young boys, are developing breasts at an alarmingly young age, and adolescent girls are starting their menses as early as age 7 or 8.

What Are Some of the Symptoms of Estrogen Dominance?

For adult women, estrogen dominance leads to weight gain, especially in the breasts, waist, and mid-section of the body. Other symptoms of estrogen dominance (or not enough progesterone) are listed as follows: Hypothyroidism, high cholesterol, joint pain, mood swings, PMS, irregular or heavy bleeding during the menstrual cycle, menstrual cramps, endometriosis, uterine leiomyomas (firbroids), polycystic ovaries, sweet cravings, decreased libido, bloating, migraines, cold hands and feet (because of hypothyroidism), hair loss, low metabolism (because of hypothyroidism), foggy thinking, memory loss, early signs of aging, weight gain without change in diet or exercise (because of hypothyroidism), lack of motivation, irritable bowel syndrome.

How Do You Treat Estrogen Dominance?

Estrogen dominance is often treated with supplementation of progesterone (natural progesterone cream) or other hormones as determined by saliva testing. Changes in diet are another effective treatment of estrogen dominance. Adding fiber helps eliminate estrogen from the body. Eating a diet of organic fresh fruits and vegetables and moderate amounts of organic, hormone-free, antibiotic-free meat reduces the number of hormones and pesticides consumed. Removing all dairy products will help. These contain hormones and pesticides as well. (Pesticides are also xeno-estrogens). Eating this diet and exercising will lower body fat, leading to lowered estrogen levels. Women who are estrogen dominant are also frequently insulin resistant. Removing/restricting the refined carbohydrate intake and balancing the diet with hormone-free proteins, organic vegetables, low-glycemic fruits, and plenty of water will change many of the symptoms of estrogen dominance over time.

Natural Progesterone Cream is often used to balance out the excess estrogen.

Chaste Tree (also called Vitex) is considered THE herb of choice to promote regular menstrual cycles, normal bleeding, and reducing menopausal symptoms.

Red Raspberry supports normal menstruation and healthy menopause and is rich in the minerals calcium, magnesium, and iron. It supports alleviation of menstrual cramps and hot flashes and encourages normal blood flow.

Dong Quai has been used for thousands of years in China to promote normal and pain-free menstrual cycles. It alleviates hot flashes and vaginal dryness during menopause and may help stabilize blood sugar levels, normalize sleep patterns, and promote calmer moods.

Red Clover Blossoms are the richest source of phytoestrogenic isoflavones, which support normal and healthy estrogen levels in women. This herb helps to balance the estrogen levels in the body, removing excess estrogens over time as needed.

For additional information that may help, see the PMS page.

back to top

Natural Treatment for Hypothyroidism


Nutrients and Supplements

(take as directed on label)

Iodine - Iodine is used along with tyrosine to make thyroid hormone. This is not the only function of iodine in the body. More can be read in the article "Iodine in the Body". Sources of iodine include Lugol's solution, seafood, and kelp. Some can be found in asparagus, garlic, lima beans, and sesame seeds. There are many other sources of iodine, but many that are listed as sources are also considered to be goiterogenic foods.

L-Tyrosine - Tyrosine attaches to iodine atoms to form active thyroid hormones. Therefore, it in not surprising to know that low levels of tyrosine have been associated with hypothyroidism. Tyrosine is important to overall metabolism. It is also a precursor to adrenaline, norepinephrine, and dopamine. These neurotransmitters regulate mood and when deficient can lead to depression. Tyrosine also acts as a mild antioxidant, suppresses appetite, and helps to reduce body fat.

Selenium - Selenium is deficient in about 50% of people's diets. those living in areas of the world where selenium is deficient have a greater incidence of thyroid disease. While a selenium deficiency does not decrease the conversion of T4 to T3 in the thyroid or the pituitary, it does result in a greater decrease in its conversion in the other cells of the body. People with a deficiency of selenium usually (usually!) have elevated levels of T4 and TSH. The trace minerals zinc, copper, and selenium are the required cofactors for iodinases (the enzyme which converts T4 to the far more active T3).

Essential Fatty Acids - These are necessary for the proper function of the thyroid gland. Every living cell in the body needs essential fatty acids for rebuilding and producing new cells. You can not produce hormones without them. There are two basic categories of essential fatty acids, Omega-3 and Omega-6. Omega-3 fatty acids include alpha-linolenic and eicosapentaenoic acid (EPA). They are found in fish, flaxseed oil, and walnut oil.

Zinc - Zinc is the second most common mineral deficiency and has been shown to re-establish normal thyroid function in hypothyroid patients who were zinc-deficient, even though they had normal serum T4 levels. The trace minerals zinc, copper, and selenium are the required cofactors for iodinases (the enzyme which converts T4 to the far more active T3).

Progesterone - Natural progesterone cream has been shown to increase thyroid activity in people who have estrogen dominance. For more information see the article "Estrogen Dominance and Hypothyroidism".


Avoid fluoride* (including that found in toothpaste and tap water) - Chlorine, fluorine, and fluoride are chemically related to iodine, and compete with it, blocking iodine receptors in the thyroid gland. Up until the 1950's, doctors in Europe used fluoride in people that had OVERactive thyroids (HYPERthyroidism). Research on fluoride is being openly acknowledged as the cause of thyroid cancer, Kaschin-Beck disease and iodine deficiency. For instance, in the Journal of Clinical Endocrinology, Volume 18, 1958, page 1102, Drs. Galetti and Goyer explain the "Effect of Fluorine in Thyroidal Iodine Metabolism in Hyperthyroidism." Three-quarters of the world's population is suffering from iodine deficiency in areas, which are identical to endemic fluorosis areas. Out of the over 150 symptoms and associations of hypothyroidism, almost all are also symptoms of fluoride poisoning.

How does fluoride effect the thyroid? First of all, the process of making thyroid hormone is greatly slowed down. Fluoride block tyrosine and iodine from coming together to form thyroid hormone. Secondly, fluoride blocks how cells take in the thyroid hormones. Thirdly, fluoride inhibits thyroid stimulating hormone (TSH) from being released by the pituitary gland. Lastly, fluoride blocks the thyroid gland's own receptors for TSH inhibiting its actions.

The phosphoric acid used in soft drinks can also contain fluorine, which is equally implicated.

Mercury - Mercury is an endocrine disrupter. Autopsy studies in 1975 revealed that, contrary to accepted belief that the kidney was the prime accumulator of inorganic mercury, the thyroid and pituitary retain and accumulate more inorganic mercury than the kidneys. Studies have documented that mercury causes hypothyroidism, damage of thyroid RNA, autoimmune thyroiditis (inflammation of the thyroid), and impairment of conversion of thyroid T4 hormone to the active T3 form. Mercury causes many problems in the body, but our focus here is hypothyroidism. Therefore, the mercury of most concern is in dental fillings and vaccines. These are the two most common sources you are likely to encounter.

Avoid chlorine (like that in pools and tap water) - Chlorine, fluorine, and fluoride are chemically related to iodine, and compete with it, blocking iodine receptors in the thyroid gland. Animal research has shown that moderate levels of chlorine and its by-products have been shown to affect red blood cells, thyroid function, and development. A significant decrease in serum thyroxine (T4) was reported following 4 wk exposure to chlorine at 0.1 g/L of drinking water. A depressive effect of chlorate and chlorite ions on thyroid hormones was observed. Several studies have associated decreased T4 level with increased binding of iodide to gastrointestinal tissue. These observations led to the hypothesis that chlorine or its by-products oxidize iodine in food to a reactive species that binds to tissues of the digestive tract, blocking iodide uptake into the thyroid follicles and reducing the synthesis of thyroid hormones.


Eat very little if any of the following foods: Broccoli, Brussels sprouts, cabbage, kale, mustard greens, peaches, pears, radishes, spinach, and turnips. These foods suppress the function of the thyroids. If you have severe hypothyroid symptoms, then you should completely eliminate these foods.

Avoid processed and refined foods.

Eat more of the following foods: Apricots, dates,molasses, parsley, potatoes, prunes, raw seeds, and fish.

Drink steam distilled water only (this is the best way to avoid fluoride and chlorine).

back to top

Lugol's Solution

(2 drops = 12.5 mg)

Lugol's iodine, also known as Lugol's solution, first made in 1829, is a solution of iodine named after the French physician Jean G.A. Lugol. Lugol's iodine solution is often used as an antiseptic and disinfectant, a starch indicator, to replenish iodine deficiency, to protect the thyroid gland from radioactive materials (e.g. "fallout"), and for emergency disinfection of drinking water.

It consists of 5% iodine (I2) and 10% potassium iodide (KI) in distilled water with a total iodine content of around 130 mg/mL. Potassium iodide is added to render the iodine water-soluble.

Tests Using Lugol's Solution

There are two tests, that I am aware of, that are supposedly used to measure iodine defficiency. These two tests are the skin patch test and the iodine loading urine test. Let us look at each test from a physiological standpoint and try to determine their legitimacy.

The Skin Patch Test

There is a local Naturopathic doctor who has a weekend radio show and was one day explaining how to do a thyroid test using Lugol's solution. He stated that if you paint a 50 cent piece size spot on your skin, and measured how long this took to disappear that it would tell you if your thyroid was underactive and that your body needed iodine. He stated that once this iodine stain was on the skin that it should last for up to 3 to 4 days. If it didn't last that long, one was to repeat this procedure daily until it did last that long.

From a standpoint of physiology, this test seemed questionable. I contacted this doctor and asked for an explanation on the mechanism for this test. The only reply that I received was, "..the more iodine the body needs, the more it absorbs". Not the answer I was asking for.

My point of view was the opposite of what he was proposing. If the body needs iodine, odds are the thyroid is underactive. If the thyroid is underactive, then the metabolism of the body (including the skin) will be underactive. Given this, anything placed on the skin (a metabolically underactive skin) would take longer to dissipate and would not be removed as quickly. Highly metabolic skin (as with normal or overactive thyroid) would have its normal blood flow and moistness to readily remove the substance from the area.

It may be that the dry skin experienced in hypothyroidism will quickly absorb any liquid that touches it. In this case, the skin would be like a dry sponge and would quickly dissipate the solution. Once the thyroid has been boosted to normal, the skin would then change to a more normal, moist skin and would have a less rapid absorption of the iodine patch, as a wet sponge would have trouble accepting more water.

Unless there have been iodine receptors recently discovered on the skin, which are upregulated by the thyroid in times of need , I am lost on how this test is of any value. Until this skin patch test mechanism is explained to me properly, I have doubts about its validity.

If anyone has the answer, please contact me.

Meticulous research by Nyiri and Jannitti in 1932 showed clearly when iodine is applied to the skin in almost any form, 50% evaporates into the air within 2 hours and between 75 and 80 percent evaporates into the air within 24 hours. (1) A total of 88 percent evaporates within 3 days and it is at this point that the evaporation stops. The remaining 12 percent that is absorbed into the skin has several fates. Only 1-4% of the total iodine applied to the skin is absorbed into the blood stream within the first few hours. The rest of the iodine within the skin (8-11%) is slowly released from the skin into the blood stream.

I have questions on the validity of this research as well, but it does give some helpful information.

As a test for thyroid function and iodine defeciency, the iodine skin patch test is questionable.

On the other hand, the use of iodine on the skin for other purposes is of great value. This will be discussed in the Iodine in the Body article.

The Iodine Loading Urine Test

In Dr. David Brownstein's book, Iodine: Why You Need It; Why You Can't Live Without It, he summarizes his own clinical experience with hundreds of patients for whom he has prescribed iodine with excellent results and minimal side effects. To determine whether a patient is iodine sufficient, he uses the iodine-loading test described by Dr. Abraham and now in use at the Schachter Center. This was the test that Abraham used to determine if a person had an optimal amount of iodine in his/her body. Other research had shown that iodine is readily absorbed when ingested orally and readily excreted in the urine. The assumption was that if a person ingests a given amount of iodine and is iodine sufficient, most of the iodine should be found in the urine over a 24-hour period. On the other hand, if the person does not have an optimal amount of iodine in his body, when he ingests the iodine, his body will tend to hold onto it and a smaller amount will be found in the urine during the 24-hour collection period.

To do this test, a patient first empties his bladder and then ingests 50 mg of iodine/iodide (to be discussed further below). The patient then collects his urine for the next 24 hours and a sample of it along with a note that includes the total volume collected is sent to an appropriate laboratory. If the person excretes 90% or 45 mg of the iodine, he is considered iodine sufficient. If less is excreted, the patient is not optimally sufficient or is iodine insufficient and a therapeutic dosage of iodine may be administered for a period of time, after which the test is repeated. Dr. Brownstein has found in using this test, that more than 90% of his patients are iodine insufficient. Once a person is iodine sufficient, the maintenance dose for an adult to maintain sufficiency is about 12.5 mg of iodine/iodide daily. The treatment dose when a person is iodine insufficient is generally between 12.5 mg and 50 mg daily. Preliminary research indicates that if a person is iodine insufficient, it takes about 3 months to become iodine sufficient while ingesting a dosage of 50 mg of iodine and a year to become iodine sufficient while ingesting a dosage of 12.5 mg of iodine daily. However, the patient needs to be monitored closely with awareness of possible side effects and detoxification reactions

Obviously this test would not be an easy "at home" method of determining iodine need.

Lugol's and Gout

The connection between hypothyroidism and gout makes it understandable why Lugol's Iodine was used to treat gout in the past. It was done by 'painting' the soles of the feet with two drops of Lugol's before retiring for the night allowed the body to absorb what it needed from the soles. If, upon waking, the Lugol's was gone it meant that the body had taken what it needed and needed more. Painting was done on a nightly basis and as treatment progressed, the need for the solution diminished because the body rebuilt its stores and thus absorbed less and less over each 24 hour period until none was absorbed at all.

back to top

Iodine in the Body

There are basically two forms of iodine used in the body. One is organic iodine and the other is inorganic. Below is a table explaining the each form and whether or not it is toxic.

Forms Toxicity

A) Inorganic

1) Non - radioactive

a) Lugol Solution Extremely safe

b) tincture of iodine Extremely safe

c) iodides (i.e., SSKI) Extremely safe

2) Radioactive iodides for diagnostic Carcinogenic and Cytotoxic

and therapeutic purposes

B) Organic

1) Naturally occurring

a) thyroid hormones Safe within Physiological ranges

b) thyroidal iodolipids Safe within Physiological ranges

2) Man made

a) radiographic contrast media Extremely toxic

b) iodine - containing drugs Extremely toxic

(i.e., amiodarone)

Thyroid hormones are not the only place that iodine is used in the body. Iodine serves many functions throughout the body. The recommended dietary intake of 100-150 mcg is perhaps 100 times too low for the purposes of the entire body use. This Recommended amount only reflects the lever needed to keep the thyroid from becoming underactive. The potential benefits of using higher amounts include enhancement of the immune system function, reducing the incidence of breast cancer and possible fibrocystic breast disease.