The Thyroid Gland: Anatomy & Physio...

The Thyroid Gland: Anatomy & Physiology

The Thyroid Gland: Anatomy & Physiology

Michelle Steinberg

Spring 2008

Introduction: Hypothyroidism

The Thyroid Gland: Anatomy & Physiology

The thyroid gland is butterfly shaped and sits on the trachea, in the anterior neck. It is comprised of two lobes connected in the middle by an isthmus. Inside, the gland is made up of many hollow follicles, whose epithelial cell walls (also known as follicle cells) surround a central cavity filled with a sticky, gelatinous material called colloid. Parafollicular cells are found in the follicle walls, protruding out into the surrounding connective tissue.

The thyroid is the largest exclusively endocrine gland in the body.  The endocrine system is the body’s communication hub, controlling cell, and therefore organ, function. A primary goal of the endocrine system is to maintain homeostasis within the organism, despite external fluctuations of any sort.  Hormones, which act as chemical messengers, are the mechanism for this communication.

The hormones secreted by the thyroid gland are essential in this process, targeting almost every cell in the body (only the adult brain, spleen, testes, and uterus are immune to their effects.)  Inside cells, thyroid hormone stimulates enzymes involved with glucose oxidation, thereby controlling cellular temperature and metabolism of proteins, carbohydrates, and lipids.  Through these actions, the thyroid regulates the body’s metabolic rate and heat production.  Thyroid hormone also raises the number of adrenergic receptors in blood vessels, thus playing a major role in the regulation of blood pressure.  In addition, it promotes tissue growth, and is particularly vital in skeletal, nervous system, and reproductive development. [See Handout 1 & 3, taken from Human Anatomy and Physiology; Marieb & Hoehn, 620-21, for anatomical drawings and details of thyroid’s effect on specific body systems.]

The two major thyroid hormones (TH) are unique in that, unlike most hormones, they are neither protein nor cholesterol based.  Instead, they incorporate iodine as an active constituent; the amount of iodine differentiates between thyroxine (also known as tetraiodothyronine or T4) with four iodine molecules and triodothyronine (T3) with, predictably, three iodine molecules. While T4 exists in greater abundance than T3 in the body- thought to be at a fifty to one ratio, T3 is considered to be ten times more active. There is much debate about the physiological difference between the two hormones.  It is currently thought that T4 may act as the reserve form, having a more direct role in the hypothalamus/pituitary negative feedback loop, while T3 has a more dynamic physiological effect in the body.  Others suggest that both have a critical part in physiological activity.

TH (particularly T4) is synthesized in the gland’s colloid filled lumen from the combination of the glycoprotein thyroglobulin and stored iodine atoms.  This process involves six interrelated steps that are initiated when thyroid stimulating hormone (TSH), released by the pituitary gland, binds to follicle cell receptors.  Thyroglobulin is then made in the follicle cells from tyrosine amino acid and discharged into the lumen where it becomes part of the colloid mass.  Follicle cells are simultaneously trapping iodide (the element’s form most readily available in food) from the blood stream- retrieving it via active transport from the lumen.  There, the iodides are converted to iodine as electrons are removed through oxidation.  Within the colloid, the iodine then attaches to tyrosine amino acid on the thyroglobulin molecules. When one iodine attaches to the tyrosine, monoiodotyrosine (T1) is formed; the bonding of a second iodine creates diiodotyrosine (T2).  Enzymes then link T1 and T2- two T2 makes the hormone T4, while a T1 and a T2 leads to the hormone T3.  Follicle cells then recover the hormones, where they pass through an enzymatic process and are then released into the bloodstream.  However, the majority of the body’s T3 is made directly on the tissue level, as target cells use enzymes to remove one iodine atom from the T4 molecules made in the thyroid, converting them to T3 before use.   Most of the alteration occurs in the liver, using enzyme 5-deiodinase. (See Handout 2 for a diagram of TH production (taken from Human Anatomy and Physiology; Marieb & Hoehn, 622.)]

In its behavior, TH functions somewhat similarly to steroid hormones.  As it  is not water soluble, it requires a protein-based molecule for transport throughout the blood stream. T3 and T4 will generally pair with thyroxine binding globulin (TBG) for this purpose, though they can also use albumin and prealbumin.  At any given moment, the vast majority of TH in the body is in this bound, and essentially inactive, state, either in route or awaiting transport.  The small percentage of unbound, physiologically active hormone is called “free” T3 or T4.   It appears that TBG and albumin have higher affinity for T4, which could explain T4’s higher levels in blood and its slower metabolism, and perhaps account for free T3 being the more physiologically active substance.   The main site of TH degradation is in the liver and its primary elimination is via kidneys (80%, the other 20% is via the colon.)  (http://www.levoxyl.com/pi.asp.)

When TH enters a cell, it attaches to receptor sites in various locations. Within the cytoplasm, it primarily connects to the mitochondria, where it helps control cellular metabolism through oxidative phosphorolation.  During this process the mitochondria use oxygen to generate energy as ATP (Adenosine triphosphate); heat is released as a byproduct of this reaction.  Thus, the thyroid (under higher regulation as we will see below) controls body temperature and food metabolism through its role in stimulating mitochondrial activity.  TH also enters the cell nucleus where it binds to DNA; here it precipitates gene transcription, and the synthesis of messenger RNA and cytoplasmic proteins.  Other hormones, including Growth Hormone (GH) and Prolactin, also depend on the presence of TH to exert their own effects on cells; the absence of TH inhibits their activity. (E. Kopf, “The Thyroid Gland,” p. 5-6 and http://www.levoxyl.com/pi.asp.)

Messages from the anterior pituitary gland are the main stimulus for the action of the thyroid gland.  The pituitary gland, in turn, is triggered from above by the hypothalamus.  The three organs are connected in a negative feedback loop that involves their vigilant monitoring of and response to the levels of TH in the blood, as well as other internal and external stimuli; this relationship is sometimes referred to as the hypothalamic-pituitary-thyroid axis.  The hypothalamus secretes protein hormone thyrotropin-releasing hormone (TRH), which heads directly to the pituitary gland via the hypophysial portal blood system, stimulating the release of TSH.  TSH then moves through the bloodstream, binding with receptors in the thyroid gland, prompting the secretion of TH into the blood.   Both T4 and T3 then exert a negative feedback effect on the hypothalamus and pituitary- an increase in their blood levels lowers the amount of TRH and TSH secreted and a decrease in their levels causes a rise in the TRH and TSH. Stimuli to the higher brain including temperature and stress can also effect TRH production in the hypothalamus; for instance, cold temperatures can increase the body’s requirements for TH as more internal heat will be need to maintain homeostasis and the hypothalamus reacts accordingly. Stress affects the thyroid gland not only through the hypothalamus, but also directly via the sympathetic nervous system.  There are sympathetic nerves that connect with the gland; during their stimulation in times of stress, they trigger increased TH release. In addition, it appears that epinephrine from the adrenal gland can also act directly on the thyroid.  (E. Kopf, p. 3)

Diet can effect thyroid function, as a high calorie/high carbohydrate diet can lead to increased conversion of T4 to T3- a mechanism that likely assists in keeping an organism’s weight stable.  Meanwhile, prolonged fasting can result in a decrease in T3 production- which may be adaptive for conditions of food scarcity, slowing down the body’s metabolism and energy consumption. (E. Kopf  p.6)

(Marieb & Hoehn were referenced in the section above, unless otherwise cited.)

 

Hypothyroid: Signal Lost

 

If the thyroid gland produces too little or too much TH, a number of the body’s functions will be adversely affected. The production of excess TH is called hyperthyroid; corresponding to the hormonal overabundance, the pituitary will generally slow secretion of TSH, as the blood levels of T4/T3 signal the presence of too much of the hormones.  Here, the focus is on the opposite condition, hypothyroid, when the thyroid is not releasing enough TH to satisfy the body’s needs.  In this case, the pituitary increases discharge of TSH, in an attempt to stimulate the thyroid to provide more TH- a demand it is unable to fulfill.  It has been estimated that 13 million people in the U.S. suffer from hypothyroidism; the condition is more prevalent in women (approx. 5-8 times more likely than men), among whom it is estimated that a minimum of 1 in 8 will develop a thyroid disorder in her lifetime. (http://utdol.com; & M. Shomon, p.1)   The incidence increases with age; approximately 20% of post-menopausal women are diagnosed with hypothyroidism.  Further, these statistics can be somewhat misleading, as many cases go undiagnosed and/or a person may have subclinical hypothyroidism, where one may suffer associated symptoms despite having a technically “normal” T4 level and only “mildly” elevated TSH. (http://www.womentowomen.com/hypothyroidism/)

A hypothyroid pathology can be broken into three different categories: primary, secondary, and tertiary. Primary hypothyroidism (which will be the main concern of this paper) is when the root of the dysfunction lies within the thyroid gland itself.   Though pituitary and hypothalamic action will certainly still impact the condition, they are not the primary cause. Secondary hypothyroidism is when the problem can be traced to the pituitary gland, and tertiary is when the hypothalamus is causing the condition.  Primary hypothyroidism is significantly more common, comprising approximately 95% of cases.

There are several conditions that can result in primary hypothyroidism.  The main cause worldwide, though it is often considered to be of lesser concern in the U.S. (a position sometimes disputed, as discussed below) is iodine deficiency. As the thyroid depends upon ingested iodine to form TH, a shortage of iodine in the diet can result in hypothyroidism.  It is estimated that over 200 million people around the world are hypothyroid for this reason.  Too much iodine, on the other hand, can also be problematic, as it can be a signal to inhibit the conversion of T4 to T3- ultimately, resulting in hypothyroidism as well.

Thyroiditis- of which there are several types- is another leading cause.  Thyroiditis is a general term for an inflammation of the thyroid gland.  The inflammation destroys thyroid cells (at a varying rate depending upon the condition), rendering the gland unable to produce the necessary amount of TH, thus leading to hypothyroidism.  Thyroiditis is often caused by an autoimmune condition- by far the most common of which in the U.S. is Hashimoto’s Thyroiditis- also know as chronic lymphocytic thyroiditis.  Women are fifteen to twenty times more likely than men to develop this condition. An autoimmune thyroid condition occurs when the immune system mistakenly attacks healthy thyroid cells.  Cases of thyroid autoimmunity generally start with T and B white blood cells- the primary infection fighting immune cells: 1) first, T and B immune factors enter the thyroid gland; 2) T cells mistakenly identify molecules that are part of the body’s own cells as invaders; B cells then produce autoantibodies that attack these cells; 3) usually these antibodies then attack thyroid peroxidase, a thyroid protein, and this seems to result in the destruction of thyroid cells.  There are many theories- but few solid conclusions- as to why this undesirable process begins.   Some current ideas include:

-          Antibodies, used during an infection by a virus that has a protein similar to a thyroid protein, may then mistakenly target the body’s own thyroid cells that too closely resemble the invader.

-          A gene may interact with thyroid cells triggering a self-destructive response, inflammatory or other.

-          Fetal cells accumulated in a mother’s thyroid gland may precipitate an immune response, leading to autoimmune thyroiditis during or following pregnancy.

-          Excess iodine is sometimes thought to trigger the process leading to Hashimoto’s.

(http://www.umm.edu/patiented/articles/what_causes_hypothyroidism_000038_2.htm)

Subacute thyroiditis is a temporary condition that occurs in three phases: hyperthyroidism, hypothyroidism, followed by a return to normal thyroid function.  In such cases, a person may feel extremely sick and exhibit symptoms of both hypo and hyperthyroidism.  Symptoms generally last 6-8 weeks, but in about 10% of cases chronic hypothyroidism may result.  This condition occurs in up to 10% of pregnant women, manifesting around 4-12 months after pregnancy.  It can also occur on occasion in men and women of all ages.

A goiter may occur in hypothyroidism whether caused by iodine deficiency, an autoimmune condition, or another less common cause.  Goiters are enlargements of thyroid glands that appear as cyst-like or fibrous growths on the neck; they can vary greatly in size.  Treatment of the underlying condition can reduce the goiter’s size, but will not often lead to its total disappearance. If goiters pose a threat of constricting the airway, they are usually surgically removed.  (www.thyroid.org)

Hypothyroidism also commonly results from the treatment of hyperthyroidism or thyroid cancer. Hyperthyroid individuals often receive radioactive iodide treatments in an attempt to ablate the gland- stemming the oversecretion of TH.  More than half of the patients in this category develop permanent hypothyroidism within a year of therapy, and up to  65% do after five years.  These individuals require thyroid replacement therapy for the rest of their lives; it is important to note that no alternative therapies can substitute for hormone replacement in such situations.  Other treatments for hyperthyroid include surgery or antithyroid drugs and can result in hypothyroidism as well.  In cases of thyroid cancer that involve total removal of the gland, lifetime treatment with thyroid hormones is also necessary.  When only one of the two thyroid lobes is removed, hypothyroidism is less common, as the remaining portion of the gland can sometimes compensate for the loss.

Certain drugs will trigger hypothyroidism by various physiological mechanisms.  Lithium, for example, affects thyroid hormone synthesis and secretion. 50% of people who take lithium may develop a goiter- 20% of those likely have symptomatic hypothyroidism, and 20-30% asymptomatic. See Handout 4 (from http://www.levoxyl.com/pi.asp) for a fairly comprehensive list of drugs that impact thyroid function.  Radiation treatments (due to cancers of the head and neck) and congenital hypothyroidism in babies are two other possible causes of hypothyroidism.

(Except where otherwise noted, the information on hypothyroid pathology referenced: http://www.umm.edu/patiented/articles/what_causes_hypothyroidism_000038_2.htm)

 

A Broad Spectrum of Symptoms…

 

When the body does not produce adequate levels of thyroid hormone to fulfill its needs, a host of major, but sometimes hard to categorize, symptoms can occur.  Advanced hypothyroid syndrome leads to myxedema, which literally means “mucous swelling.”  The term was coined in 1877, when a doctor in London performing an autopsy first recognized the connection between mucous logged tissue, atherosclerosis, and an enlarged, non-functioning thyroid gland. (Stephen Langer & James Scheer, The Riddle of Illness, p. 8)  The other most prominent symptoms of this condition are graver versions of those found in many mildly hypothyroid individuals, including: thick, dry skin and puffy eyes, lethargy, low metabolic rate, coldness, constipation, and mental sluggishness.  Handout 2 gives an overview of the physiological effects of TH secretion- the following is a more specific summary of the effects of hypothyroidism, grouped by body system:

-          The body’s inability to promote normal hydration and regular skin secretions leads to pale, thick, dry skin, edema- all over, but particularly in the face, and coarse, thick hair and nails. Loss of head hair and lateral eyebrows can occur.  Skin is often pale or yellow toned. There is decreased sweating.

-          The following signs occur due to a decreased basal (resting) metabolic rate, inability to use oxygen effectively, and decreased action of the sympathetic nervous system:  body temperature is low, accompanied by cold intolerance; weight gain occurs despite a decreased appetite; there is reduced sensitivity to catecholamines. Generalized lethargy and fatigue are common.

-          There is decreased efficiency of the heart’s pumping mechanism, leading to a lower heart rate (bradycardia) and, commonly, low blood pressure.  Breathing can be labored and shallow.  Heart palpitations and irregular extra beats may occur.  (Note: on some occasions, mild high blood pressure can also present, due to slowed pumping combined with increased stiffness of blood vessel walls.) Poor circulation is frequent and, correspondingly, cold hands and feet. There is a common overlap between hypothyroidism and heart problems.

-          There is a disruption of carbohydrate, lipid, and protein metabolism; thus glucose metabolism is decreased, cholesterol and triglyceride levels may be elevated in the blood, and protein synthesis is decreased. The overall increase in cholesterol can transpire as an increase in LDL and decrease of HDL; this increase in blood cholesterol, combined with decreased efficiency of the heart/circulation, leads to an increased rate of atherosclerosis in hypothyroidism. (http://jcem.endojournals.org/cgi/content/full/88/6/2438)

-          GI motility, tone, and secretions are decreased, leading to possible constipation and malabsorption.

-          In a child’s nervous system, lack of TH can lead to deficient brain development; in adults, there can be a slowing of mental processes and a lack of clarity, slow speech, memory loss, nervousness, and depression.

-          Muscular development and function is impaired (in part due to decreased protein synthesis) leading to sluggish muscles action, cramps, and myalgia. There is increased incidence of fibromyalgia and carpal tunnel syndrome.

-          Skeletal growth and maturation is impaired in children; joint pain occurs in adults.

-          In women, ovarian function and lactation are depressed.  This can lead to sterility. Menstruation may be painful and excessive. Overall reproductive function may be suppressed in men as well.  Libido in both may be decreased (related to lack of energy and the involuntary prioritization of body functions in times of metabolic scarcity.)  Sexual sensation may also be decreased as a result of poor circulation.

-          Changes in vocal cords (and overall system dryness) may lead to a characteristic hoarseness of the voice.

-          Headaches, possibly related to several of the above physiological changes, are also common.

(Marieb & Hoehn, p.621; Eric Kopf, M.D. “The Thyroid Gland”, p. 8)

Given the vast array of symptoms, it is critical to recognize that a given individual is not likely to show all of them, and certain signs may be more or less prominent in any specific case.  In addition, people may manifest opposite symptoms.  For example, one endocrinologist noted that at certain times, individuals of a smaller overall body type may lose, instead of gain, weight when their thyroid is underactive. Further many of the symptoms, particularly those associated with mental function, are extremely subjective in nature.  That said, it is critical, as always, to treat the individual, using the above as a general guideline to body systems that may indicate thyroid dysfunction, rather than a road map to what hypothyroidism should look like.  Perhaps the most important point is to notice the possible connection between so many seemingly unrelated symptoms.  Hypothyroid individuals, particularly those with subclinical hypothyroid, may undergo the experience of being told that their symptoms are psychosomatic, simply part of aging, or totally unrelated, before they are officially diagnosed as being hypothyroid- and this can be very frustrating, indeed. The wisdom of a person’s own experience of her condition is often going to be the most effective guide to treatment.

 

Screening for Thyroid Dysfunction

 

In the late 1930’s, before the advent of assessing thyroid levels through blood testing, Broda Barnes M.D. initiated the use of the Barnes Basal Temperature test.  This simple test is easily performed on oneself at home.  First, shake down a standard thermometer before going to bed; immediately after waking, leave the thermometer under an armpit for ten minutes.  If the temperature is between 97.8 to 98.2, thyroid function is probably normal.  If the temperature is lower, retest the following day.  If the temperature is again low, the thyroid gland is likely under functioning. Dr. Barnes reported tremendous success using the outcome of this test to identify hypothyroidism in individuals exhibiting common symptoms.  (Langer & Scheer, p. 3)  There is some controversy surrounding the accuracy of the test.  One endocrinologist states that the amount of thyroid replacement hormone that would be needed to raise one’s basal temperature would far exceed an adequate replacement dose.  Thus, a low basal temperature will probably persist in some individuals despite the taking of thyroid replacement. (Kopf, p. 3)   Current proponents of the Barnes Basal Temperature test nonetheless see it as a useful mechanism to discern a low functioning thyroid, particularly in cases where the symptoms are present, but clinical tests may not register the dysfunction- or may label it as subclinical.

Thyroid stimulating hormone (TSH) level is the most frequently used laboratory test for gauging thyroid function.  As discussed earlier, when the thyroid gland produces inadequate supplies of TH, the pituitary secretes a greater amount of TSH in an attempt to increase the TH level.  Thus, in someone who is hypothyroid, the TSH value would be higher than “normal”. In adults, many western doctors rely exclusively on this test, checking other levels only when the TSH is high or low.  In children, it is most likely combined with “free” T4 screening from the outset.  (http://www.levoxyl.com/pi.asp)   The problem with this test is primarily the range of “normal” TSH; for many years anything between .2 and 5.5 was seen as the desired level.  In recent years, some endocrinologists have begun to think of 2.5 as a more accurate upper limit. It is likely that the range of the test may eventually be moved to reflect this opinion.  Suddenly many people who were previously seen as euthryoid (having a “normal” functioning thyroid) will be clinically hypothyroid.  In fact, many of these people may have suffered symptoms related to hypothyroidism for years and gone undiagnosed.

Further, some doctors believe that 1 is actually the target level for TSH, which suggests that patients suffering from hypothyroid symptoms with TSH levels hovering around 2.5 may even be hypothyroid.  Another major concern is the variability among individuals.  The optimal TSH for one person may be .8, such that if it goes up to 2.0, he will experience the discomfort of hypothyroid symptoms; where as 2.0 might be standard for another person.  Ideally, there would be routine screening so that a norm would exist for the individual and it would, therefore, be noticeable when deviation occurs.  However, this is not likely to happen in the age of insurance companies and for profit medicine.  Of further concern are natural variations in one’s TSH level, which are rarely accounted for in screening or treatment. These include fluctuations based on the season, time of day, and, for women, place in the menstrual cycle.  (Shomon, p. 253)

In hypothyroid individuals who are just beginning thyroid hormone replacement therapy, doctors generally test TSH (and possibly T4/T3) every six to eight weeks until the person appears to be stable at a particular dose.  At that point, screening usually occurs every six to twelve months, unless there is a resurgence of symptoms. The reappearance of common hypothyroid symptoms may indicate that the medication dose is too low, while the presence of hyperthyroid symptoms suggests that the dose may be too high; the individual will then receive blood work to explore these possibilities.

Free T4 and free T3 tests assess the level of unbound thyroid hormones in the body.  As the majority of TH is bound, these test are assessing the smaller percentage that is more biologically active.  Often doctors, after receiving high or low TSH results, will order only free T4, through which they will confirm a hypo or hyperthyroid diagnosis (though symptomatic or developing subclinical cases can exist regardless of a normal free T4 level.) (Kopf, p. 7.)   In a medical environment where there is pressure from insurance providers to keep screening to a minimum, this has become the routine.  However, it is probably ideal to run all three tests (TSH, free T4, and free T3), at least when initially diagnosing a condition, and then on occasion, if not every time, when monitoring someone already known to have thyroid issues.  For example, some individuals may specifically have trouble converting T4 to T3, a condition that will go unnoticed without free T3 screening.  The current range for free T4 is .8-1.8 and free T3 is 230-420.

There are several other thyroid tests used somewhat less commonly and for more specific diagnosis. The radioactive iodine uptake scan (RAIU) uses radio labeled iodine molecules that can be followed as they mass in the thyroid gland.  A normal reading will have homogenous distribution of the molecules throughout the gland.  In abnormal scans, there will be either areas with increased uptake- possibly signaling cancer or a hyperfunctioning condition- or spots with decreased accumulation- which can indicate benign cysts or hypo functioning problems.

Thyroid auto-antibody screening, exactly as it sounds, checks for the presence of the antibodies that would signal an auto-immune thyroid condition.  The most common anti-bodies in this case are those found in either Hashimoto’s thyroiditis or Grave’s disease (an auto-immune hyperthyroid condition.)  The thyroid stimulating antibodies test (TSAb) identifies the agent found in Grave’s disease that mimics TSH behavior by binding to cell receptors and stimulating excess TH production.  There is also screening for antithyroglobulin antibody and antithyroid peroxidase, antibodies commonly present in Hashimoto’s and sometimes occurring in Grave’s disease.  (Kopf, p. 7-8)

Thyroid releasing hormone, the hypothalamic secretion that controls TSH release, can also be screened to differentiate between primary, secondary, and tertiary hypothyroidism.  This test measures the response of the anterior pituitary when TRH is administered.  In primary hypothyroidism, there is a two to three times increase in TSH when the TRH appears; in secondary hypothyroidism, there is no rise in TSH, and in a tertiary condition there will be a noticeable delay in the rise of TSH.

 

The Meds

 

The most common course of action after a diagnosis of hypothyroidism is thyroid hormone replacement therapy.  There are several main categories of drugs that doctors may prescribe:

- Levothyroxine is the generic of synthetic thyroxine (T4).  Brands in the U.S. include Synthroid, Levothyoid, Levoxyl, Eltroxin, and PMS-Levothyroxine.  (Doctors often prefer brands over the generic due to well-founded concern over the consistency of the generic.  For the same reason, patients are generally counseled to stick to one brand once their dose is established.)

- Liothyronine is synthetic triiodothyronine (T3).  Cytomel is the brand name in the U.S.

- Liotrix is a synthetic T4 and T3 combination drug.  Thyrolar is the brand name in the U.S.

- Natural thyroid is a non-synthetic hormone composed of desiccated pig thyroid glands.  It contains T4 andT3, as well as other components found naturally in the thyroid gland.  Armour Thyroid, Naturethroid, and Westhroid are the brands available in the U.S. (Shomon, p. 65.)

From the beginning of Dr. Broda Barnes pioneering work on hypothyroidism in the 1930’s-40’s until the 1970’s, natural thyroid supplements were the primary treatment.  In the 1970’s, synthetic T4 took over as most commonly prescribed. The main argument for this change was that the natural hormone therapies were not adequately standardized and that their T3/T4 ratio might not be optimal.  (Langer & Scheer, p. 168.) Pharmaceutical companies then primarily invested in T4 replacements, throwing their tremendous force behind popularizing this treatment option.  Synthroid manufacturers in particular aimed to dominate the market.  They falsely claimed their product to possess an advantage over other brands, in an attempt to win over doctors/patients and justify Synthroid’s significantly higher cost.  This assertion bought them a major lawsuit in 1997, which cost the company billions of dollars. (Shomon, p. 256.)

In 1999, Lithuanian endocrinologists published a groundbreaking study that proved that combination T4/T3 therapies offer better results in treating hypothyroidism than T4 alone. (Langer and Scheer, p. 168)  To this day, significant controversy exists around this issue.  There have been subsequent studies that confirmed the importance of combination therapy.  There are now several treatment options involving both hormones: natural, combined Cytomel and Levothryoxine, or Thyrolar.  According to my endocrinologist’s  experience, approximately one quarter of her patients feel better on joint therapies; some other doctors would argue that the percentage is higher.   T3 seems to be primarily useful in alleviating symptoms related to mental function that persist when solely T4 is replaced.  Since it is known that some people have problems with the T4/T3 conversion, it certainly follows that the addition of readily available T3 could have a profound effect.  In cases where it is used, the T3 comprises a small percentage of the overall therapy, corresponding to the naturally occurring ratio between the two hormones in the body.   It is worth noting that Cytomel and Thyrolar are considerably more expensive than all T4 brands and there is no generic for either medication.  This likely makes the exploration of joint therapy difficult for many people as the out of pocket cost can be prohibitive and insurance companies may be less enthusiastic about this treatment approach.

It can take anywhere from several weeks to several months for a significant change in symptoms to occur once treatment begins.  As the predicable consequence of an excessive dose of TH replacement is hyperthyroidism, the beginning of treatment can be a bumpy road for many people, leading to a seesaw between hypo and hyperthyroid states until the appropriate dose is determined. It also important to note that different life phases can result in the need for more or less medication; pregnancy, for instance, usually requires women to increase their dose.

Other than symptoms associated with hyperthyroidism (which can be major), possible temporary partial hair loss during adjustment is the main short term side-effect of thyroid hormone replacement.  Loss of bone mineral density (which can contribute to osteoporosis) and heart complications are the two main long term effects of TH replacement (the latter of major concern in geriatric hypothyroid patients.) Further research is needed on both of these to determine the real risks involved.  Patients with adrenal insufficiency should be treated for that condition before beginning thyroid replacement; individuals with diabetes, heart disease, clotting disorders, and pituitary dysfunction may require adjustments of their other medications when on T4 therapy.

Doctors usually recommend that thyroid medication be consumed first thing in the morning, at least a half hour before breakfast, with a full glass of water.  However, in Living Well With Hypothyroidism, Mary Shomon suggests that if one is not feeling up to par with a current regimen, perhaps splitting the dose throughout the day could help to maintain a more consistent hormone level. A high fiber diet or fiber supplements can interfere with the bioavailability of levothyroxine.  An increased intake of dietary fiber can necessitate a higher dose of medication and can explain the need for greater than expected amounts of  replacement hormone in some people. (http://www.ncbi.nlm.nih.gov/pubmed/8636317?dopt=Abstract)

Levoxyl manufacturers offer some general information on the medication:

-There is usually 40-80% absorption of the medication (increased by fasting and adequate water to accompany the dose.)

- If lab tests continue to indicate hypothyroidism despite an apparently adequate and normally potent dose, malabsorption or drug interactions may be occurring.  See Handout 4 for a complete list of possible drug interactions.

-  Iron and Calcium supplements should be taken as far apart as possible from thyroid hormone medication as they can severely interfere with absorption.  (My dose  dropped when I followed this advice from my doctor.)

- Many of the foods listed as possible hypothyroid hazards in the nutrition section of this paper can also interfere with thyroid hormone medication. Soy poses a particular risk.

 

The key is consistency, such that once the appropriate dose is established other factors remain the same- or at least their potential effect is recognized and leads to a reevaluation of the thyroid medication dose if symptoms reappear.

 

Cause: A Macro View

 

There are myriad ideas about what causes the thyroid to function at a less than optimal level.  As explained above, there are a number of different physiological conditions, and each of those may be precipitated by a variety of different factors.  As in any discussion of its kind, there is much speculation and disagreement. Here is a look at several theories that may offer some insight into an overall understanding of cause.

First, the toxicity of our environment no doubt has a significant impact on the thyroid gland.  Ryan Drum has done groundbreaking work in this area and most of the following section is drawn from several essays available on his website: “Environmental Origins of Thyroid Disease-Part 1”,  “Environmental Origins of Thyroid Disease-Part 2”,  and “Thyroid Function and Dysfunction.”  Drum notes that there has been a significant increase in the number of reported thyroid cases in recent years (in cats and dogs, as well, the former tending more towards hyperthyroid, the latter more likely hypothyroid.) While this may be due to higher recognition of the condition lately, it also seems likely that environmental changes have had an impact on this phenomenon. Drum cites as several major areas of concern: radiation, intake of chemical iodide displacers, and consumption of thyroid suppressive or disruptive substances.  His position is partially based on the idea that iodine deficiency in the U.S. is actually far more prevalent than often stated.

Iodide 127 is the element that the body naturally takes in for use in TH production; it is a chemically stable element, which is significant for its physiological uses, and has no natural isotopes. With the unfortunate advent of nuclear radiation, uranium fission produced iodide 131- an artificial radioisotope (by definition maintaining an unstable nucleus) that has been routinely released into the environment. Its instability means that I-131 has a half-life of eight days.  Drum posits that six plus decades of the diffusion of this isotope through nuclear explosions, accidents, and general operation of nuclear facilities is connected to the increase in thyroid pathology.

When the body has an ample stock of I-127, it is not likely to uptake I-131; it is only in cases of iodide deficiency that the body will readily accept the isotope.  As it is not naturally occurring and did not exist prior to the 1940’s, animals do not have any mechanism for dealing with it.  The I-131 moves into molecules, cells, and tissue where I-127 would normally be present. Drum explains, “When a thyroid hormone molecule experiences radioactive decay of one of its iodine atoms, that atom disappears with an inert gas [Xenon] suddenly left in its place; any functional event involving the thyroid hormone molecule with Iodine 131 decay will experience at least structural disruption and possibly destruction. All of the intended subsequent hormone-dependent functions will be terminated prematurely.” Since iodide deficiency world-wide is fairly routine, I-131 poses a significant danger.  Here, Drum points to the therapeutic value of maintaining an ample store of I-127 through regular seaweed consumption (see “Herbs” section for detail.)

One can imagine the devastating impact of massive amounts of I-131 dumped into the environment in cases of nuclear explosions (whether during tests or through their malicious intended use) and accidents. Following the Chernobyl disaster in 1986, there was a steady increase of thyroid disease.  The positive measures taken in Poland at the time also corroborate this scenario, as Polish citizens were supplied with various forms of I-127 supplementation and suffered a remarkably low incidence of nuclear related thyroid disease.  Yet, nuclear facilities continually emit I-131 into the environment.  This primarily occurs in periodic bursts, after which the radioactive iodide pollutes air and water, and lands on plants, where it is regularly consumed by all herbivores/omnivores.  It’s eight day half-life means that the I-131 will pose a threat as a thyroid hazard for approximately eight weeks (at which point it will have decayed.)  This also means that if incorporated into the body, its toxic decay is likely to occur internally, rather than after excretion.

Though I won’t go into detail here, X-rays should also be noted as another potential thyroid hazard.  The most flagrant use of high dose X-rays on the upper part of the body has been cut back in recent years, but many suffer thyroid disease as a result of past, now outdated, treatments for dermatological concerns and asthma/bronchitis.  The thyroid has little structural protection and is particularly at-risk to X-ray damage – something to consider as the frequent use of dental and chest X-rays and CAT scans persists.   (Drum, “Environmental Origins of Thyroid Disease- Part 2”, p. 5-6 )

Drum also points out the thyroid sabotaging effects of a variety of chemicals in the modern industrial environment.  One category is iodine displacers, which are other elements in the same family as iodine- halogens: fluorine, chlorine, and bromine.  These elements can displace or interfere with iodine metabolism.  Fluorine is commonly found in toothpaste and water supplies, chorine in water supplies and cleaning agents, and bromine in industrial emissions, pesticides, and preservatives.  Much like I-131, these had no occasion to enter the body in the past, and hence animals have developed few protection mechanisms to counter their effects.  They may put a considerable strain on thyroid metabolism.

Likewise polychlorinated biphenols (PCBs- now mostly banned, previously used in a variety of industrial applications and still present in the environment), Poly-bromated di-ethyl ethers (PBDE’s- found in flame retardants), Dihydroxybenzene (resorcinol- used in the production of rayon and nylon, and in furniture glue) , and MBTE (gasoline additive) all have a devastating effect on thyroid function.  PCB’s are thyroid hormone mimetics whose chemical structure closely resembles TH.   The other three substances are endocrine disruptors that can be strongly thyroid disruptive.  The ubiquitous presence of these chemicals in today’s environment may have a considerable connection to the growing incidence of thyroid disease.  (R. Drum, “Environmental Origins of Thyroid Disease- Part 1”, p. 4-8.)  Similarly, the widespread consumption of thyroid suppressive foods, particularly endocrine disruptors such as soy isoflavones, may have a significant effect; this will be covered in more detail in the section below on diet.

Another area in need of further exploration is the connection between the thyroid gland and other non-thyroid hormones, particularly estrogen and progesterone. There are estrogen receptors in the thyroid and, as a result, excessive estrogen can inhibit TH secretion.  It appears that the balance between estrogen and progesterone is critical; in a condition of either too much estrogen, too little progesterone, or a combination of both, estrogen dominance may occur.  Hypothyroidism is sometimes classed as a side effect of estrogen dominance.  Post-pregnancy, peri/menopause, and during the use of birth control pills or hormone replacement, instances when estrogen dominance is common, are also times in which hypothyroidism is more prevalent.  In addition, there also seems to be a link between excess estrogen and general auto-immune disease (Mary Shomon, Living Well With Hypothyroidism, p. 268 and http://www.womentowomen.com/hypothyroidism)  It might also be interesting to compare the rates of hypothyroidism between men and women, when only the latter who do not fall into any of the above groups are included in the calculations; perhaps the incidence would be more equal, confirming the heavy impact of hormonal factors upon the development of thyroid dysfunction.

Stress also has a known impact on thyroid function. Three main ways in which this can occur are through the stress response of the hypothalamus that may alter TRH secretion, from direct contact between the thyroid gland and the sympathetic nervous system, and through the effect of other hormones whose levels fluctuate in times of stress (estrogen/progesterone being no exception to this.)  Herbalist Michael Moore specifically refers to a Thyroid Stress Pattern, in which constant overtaxation of the thyroid gland to meet the body’s elevated requirements for TH due to stress, can lead to either a depressed or overstimulated state (or often a fluctuation between the two. )  Not insignificantly, these conditions may tie into either of his other two stress patterns, Adrenalin Stress or Adrenocortical Stress, both of which involve the body’s over dependence on other hormones- epinephrine or adrenal cortical and gonadal steroids, respectively.  (Michael Moore, Herbal Energetic in Clinical Practice, p. 83)  Indeed, the connection between hypothyroidism and adrenal fatigue is finally becoming more recognized within the medical establishment.  The symptoms of the two conditions are very similar and it seems that a state of adrenal exhaustion will undermine the effectiveness of commonly prescribed hypothyroid treatments. (Langer & Scheer, p. 168)  One theory holds that “adrenal stress impairs thyroid function because it causes overproduction of cortisol, blocking the efficient conversion and peripheral cellular use of the thyroid hormones…” (http://www.womentowomen.com/hypothyroidism/)

The role of reverse T3 also demands research.  Reverse T3 is an inactive form of T3, which the body seems to opt for converting to, instead of T3, during times of physical stress. It appears that both pregnancy and estrogen replacement therapy are instances associated with increased T3 concentration. There has not been sufficient research in this area, but it seems that this could be another link between stress, varied hormone balance, and thyroid activity.  (M. Shomon, p. 262-263.)

Ryan Drum offers another perspective on the stress factor: “I further believe that the situational low thyroid presentations (hypothyroidism) which seem to be initiated by a known life trauma, particularly loss of a loved one or similar grief-inducing events, are completely normal thyroid responses and very desirable components of the grief response…”   He holds that such cases should not involve thyroid specific treatment unless they are life threatening or last for more than one year.  He adds that as the understandable outcome of a culture that does not allow for a natural grief process, individuals suffer from “chronic secondary grief” in which one laments the lack of grieving, which can lead to a hypothyroid response. (R. Drum, “Thyroid Function and Dysfunction, p. 9)

The accepted medical treatment for hypothyroidism has long been the popping of a daily pill for life- a treatment that certainly benefits the drug companies and seems to stabilize the condition enough so that life threatening cases are now rare, while delivering a questionable quality of life and possibly posing some long term health risks.  The result of this scenario is that there has not been extensive research into the myriad factors that may contribute to the condition- as it is seen as neither a pressing situation nor of economic benefit (to pharmaceutical companies.)  Thus, there are many inconclusive (due to lack of research), but valid, theories as to why hypothyroidism may begin- more than there is space here to mention.  One final idea that may indicate the variety of possible triggers is the Epstein-Barr virus.  Epstein-Barr (EBV) is the virus that causes mononucleosis.  Some doctors now believe that there may be a connection between having had EBV (whose antibodies remain for the duration of one’s life) or full-blown mono and later developing autoimmune hypothyroidism.  It is unclear whether the overall exhaustion brought on by the virus may simply weaken one’s immunity or whether there is a more direct link.  In either case, the incidence of those who have had both seems to be high.  In fact, there is now some thought about the existence of other viral causes and a link to anti-viral agents or vaccines.  (M. Shomon, p. 27 & 272-273.)

 

Another Approach

 

Most of the understandings presented above use western physiology as their base; traditional Chinese medicine (TCM) has a very different take on the situation.  In classical TCM, what is identified in western medicine as thyroid dysfunction is seen as a symptom of imbalance between various organ systems.  Organs themselves are seen as part of functional systems rather than as anatomically isolated (and for this reason referred to in capital letters), so when one speaks of the Heart, Kidneys, Lungs, etc., it encompasses a broader physiological understanding than simply the organ itself.  In The Web That Has No Weaver, Ted Kaptchuk explains that instead of treating the thyroid, “[t]he Chinese physician, however, might effect a cure through treatment of the Heart or, depending on the total configuration of signs, through treatment of the Liver, Spleen, Kidneys, or some combination of these Organs.”  (Kaptchuk, p. 77)   An essential aspect of this approach is seeing each person as an individual- rather than a recognizable pathology (certainly a position shared by western herbalists).  As TCM does not necessarily identify thyroid dysfunction as such, it does not seem appropriate to offer any generalizations of TCM approaches for “hypothyroidism”.  One integrative practitioner, who combines TCM, Ayurvedic Medicine, and western physiology, uses a treatment plan that may integrate diet, exercise, herbs, medications, environment, lifestyle, and acupuncture.  She suggests four main areas that she tends to focus on herbally: 1) liver cleansing; 2) regulation of digestion and elimination; 3) spleen and stomach tonification; 4) kidney and adrenal tonification. (http://www.thyroid-info.com/articles/shasta.htm)   It appears that while Ayurvedic medicine has some similarities with TCM’s view of the body, emphasizing overall balance and harmony over the identification of specific pathologies, an Ayurvedic understanding of thyroid function/dysfunction is also somewhat more compatible with a western physiological understanding of the gland.

 

Herbs & Hypothyroidism

 

When using many of these herbs with clients on thyroid medication, blood levels must be carefully monitored, as the required medication dose may shift over time concurrent with herb use.  Herbs, like all food substances and supplements, should not be taken at the same time of day as thyroid hormone medication.

These herbs, while having the potential to help someone with a hypothyroid condition, are only one part of a multifaceted approach.  Diet and lifestyle (exercise, sleep habits, stress reduction, etc) are essential components of one’s thyroid health. Some  people will not be able to stop taking thyroid medication completely, no matter what degree of other approaches they are using; for such individuals, a decrease in med dose, through herbs, diet, and lifestyle changes may be the optimal outcome. Of course the situation varies between individuals, but it is important that neither the herbalist nor the client have rigidly unrealistic expectations.

See bibliography for complete information on sources, but for this section citation abbreviations are as follows: (DH)=David Hoffmann, Medical Herbalism; (MH)=Matthew Wood, The Practice of Traditional Western Herbalism; (RD)= Ryan Drum from his fantastic website- http://www.ryandrum.com/; (MH)=Maude Grieves, A Modern Herbal.  In addition, other websites are cited below.

 

General herbal actions that may be indicated (depending on individual case): thyroid tonics/stimulants, adaptogens, nervines, circulatory stimulants, bitters, hepatic and/or specific hepatic laxatives, cardiovascular tonics, nutritives, emollients.

 

 

Photo- www.ne.jp/asahi/marine/algae/Fucus.html

 

Seaweed- Others are useful as well, but specifically for thyroid, Fucus vesiculosus (Bladderwrack/Kelp)- Whole plant is used.  It is antihypothyroid and antirheumatic. It is most appropriate when iodine deficiency is involved- but can be of some use to hypothyroid/goiter conditions in general.  It  helps to regulate thyroid function, improving  all types of symptoms.  If obesity associated with thyroid is present, it can help weight loss.  Also used in relieving symptoms of rheumatoid arthritis- both internally and externally.  It is taken as tablet or infusion (1 cup boiling water over 2-3 tsp, 3x/day.) CAUTION: Its iodine content can also potentially cause hyper & hypothyroidism and it may interact with other thyroid treatments. Elevated urinary arsenic levels have been associated with it.  Prolonged use may reduce gastro-intestinal iron absorption (because of fucoidan’s binding properties), which can slowly reduce hemoglobin, packed cell volume, and serum FE concentrations.  Overtime can also affect NA & K absorption and cause diarrhea. Constituents: phenolic compounds, mucopolysaccharides, ester diglycerides, polar lipids, trace metals. (DH)

Charcoal derived from bladderwrack used in goiter; good for obesity associated w/ thyroid. (MG)

Ryan Drum sings the praises of seaweed consumption like no other, see his website for more detailed information. He notes that because it may take people some time to build up proper internal flora for seaweed digestion, it makes sense to eat small amounts daily over time, rather than large occasional doses. For the most part, he recommends eating it raw.  One of its major contributions to overall health, is its high nutrient content (including potassium, selenium, phycopolymers, algin, B vitamins, omega-3 fatty acids, among others.) Its iodine content and iodine protective potential (see section on Environmental Causes for more info) are unsurpassed.  The US RDA for iodine is 150 micrograms; while not everyone is in need of this level of supplementation, and over-supplementation carries the aforementioned risks, maintaining this amount from whatever combination of sources should be recognized as a mechanism to prevent I-131 intake.  On seaweeds specific thyroid effects, Drum writes:

“Brown seaweeds are the only known non-animal sources of thyroid hormones. Fucus spp of brown seaweeds have been used as treatment for thyroid disorders . The thyroid hormone present in Fucus is Di-Iodothyronine (DIT); it is weakly active if at all as a thyroid hormone in the mammalian body. Two DIT molecules are condensed in an elegant esterification reaction to produce tetraiodotyrosine(T4, Thyroxine). The organically bound iodine in Fucus may enhance T4 production by providing some prefabricated portions of T4. I have not seen any studies tracing Fucus-sourced DIT to either the thyroid gland or circulating T4.  The therapeutic effects of using powdered Fucus, 3-5 grams daily resemble the therapeutic effects of thyroxine medications: shrinking of goiters, weight loss, resolution of symptomatic non-autoimmune hypothyroidism, return of vim and vigor, lessening of psychiatric disruptions, and resolution of eczemas. This is especially true of women enduring postpartum physiological depression after several years of being pregnant and nursing one or more children.  I have seen no reports of thyrotoxicity from Fucus consumption. Women with low thyroid function, according to thyroid panel blood tests report improved test results. Any similar results from using Fucus teas will be due to inorganic iodine supply increase and probably not from DIT. DIT is not very water soluble.  Fucus is used to wean mildly hypothyroid patients off thyroid hormone medication. This can work only if the patient has a thyroid gland mass capable of making T4 and T3 in sufficient quantities to supply body needs. Those without a thyroid gland may be helped by the iodine from Fucus, alleviating the need to mine thyroid medications for iodine. This may also explain in part the alleged weight loss results from ingesting Fucus.”

On other Seaweeds, he says, “T4 and T3 have been found as the main organically bound iodine compounds in several brown seaweeds, notably Laminaria sp. and Sargassum sp. Up to 10% of Lamiarian iodine may be in MIT, DIT, T3, orT4. Even more in the less commonly available Sargassum (less commercially available; it is a rapidly expanding invasive of all temperate coasts; this may be good news for thyroid sufferers) (Kazutosi 2002). Kombu is one of the top 5 most consumed seaweeds in Japan and USA. The physiological effects of regular kombu consumption can be: resolution of coronary artery disease, healthier liver function, higher metabolic rate, faster food transit time, lower LDL cholesterol,, higher HDL cholesterol blood levels. If the thyroid hormones in kombu and Sargassum are available from food, this could turn out to be an effective treatment to replace both synthetic thyroxines and animal-thyroid medications. I assume at least some T4 and T3 get into the human body from dietary Kombu and stimulate more rapid clearing of fatty wastes from the liver, enabling more rapid removal of blood borne fatty wastes.  T4 and T3 are biphenols and are not water soluble. Oil extractions of Kombu may provide T4 and T3 as well as DIT and MIT(Mono-iodotyrosine) and be an effective thyrosupportive medicine. Powdered Fucus is mixed with olive oil as a vegan replacement for cod liver oil and seems to work as well or better than cod liver oil.”

He adds the caution that some individuals are extremely sensitive to iodine and too much may push them into hyperthyroid symptoms.  As for David Hoffman’s mention of potential problems from fucoidan, Drum mentions that the constituent can be cooked out of most edible brown algae, in necessary cases, by simmering it for 20-40 minutes in water.  Though he adds that fucoidan can be useful in reducing the intensity of inflammatory responses and promoting rapid tissue healing after wound or surgical trauma. His dosage for bladderwrack is up to 5 grams daily, one hour before regular meals. (RD)

 

 

 

Photo:www.dkimages.com/…/Withania-

Ashwagandha-5.html

 

Withania somnifera (Ashwagandha)-

Ashwagandha is hearty shrub in the nightshade (Solanaceae) family.  Medicinally, the root and berries are most widely used.  The root is utilized extensively in Ayurvedic medicine to increase overall health and longevity, while the fruit, seeds, and leaves are also applied as aphrodisiacs, diuretics, and treatments for  memory loss.  Outside of Ayurveda as well, Ashwagandha is viewed as an adaptogen, reproductive stimulant, anti-caricinogenic, and is also seen to provide symptomatic relief for arthritis.  It can also have sedative properties. Energetically, it is considered to be ‘horse medicine’, correlating with the translation of it Sanskrit name- “horse’s smell.”  Its main constituents are alkaloids and steroidal lactones. (http://en.wikipedia.org/wiki/Ashwagandha)

According to a study (on mice) at a University in India, ashwagandha root extract stimulates thyroidal activity (primarily by raising T4 levels) and also enhances the antiperoxidation (reduces the amount of lipid peroxides) of hepatic tissue. (http://www.ncbi.nlm.nih.gov/pubmed/9811169.)

Other studies have shown  that ashwagandha can maintain normal antioxidant function even during intentionally induced stress trauma, not only boosting antioxidant protection but also reducing the amount of cortisol that is released in response to stress. Excess cortisol can exacerbate a thyroid condition. In addition, ashwagandha supports antioxidant enzymes so they are less taxed, which can have a sparing effect on selenium, also indirectly supporting healthy thyroid function. (http://www.ei-resource.org/articles/related-conditions-articles/herbs-and-thyroid-function/.)

Michael Tierra’s wonderful monograph on ashwagandha (http://www.planetherbs.com/articles/ashwagandha.htm) gives the following Ayurvedic dosages: powder- 3-6 grams daily or up to 5 to 10 grams as an occasional tonic; decoction-16 to 31 grams added to heated milk; alcoholic Extract: 2 Tbsp., 2-4 times daily; mixed with ghee or honey-1 tsp. 2 times daily.

In my own personal use of the herb (at much smaller doses- approx 15 drops 2-3x/day), it does seem to have helped with some symptoms associated with hypothyroidism, as well as having ‘possibly’ contributed to lowering the required dosage of synthetic T4.

 

 

Photo:www.chilebosque.cl/herb/ceasia.html

 

Centella asiatica (Gotu Kola)- Gotu Kola has been used traditionally in Ayurveda for hypothyroidism. It stimulates circulation, and particularly improves mental function/clarity and memory, which may be slowed in cases of hypothyroidism. It is also helpful to the nervous system generally and can act as an adaptogen.  Should used in fresh preparations.  (See Christopher Hobbs: http://www.foundationsofherbalism.com/HerbWalk/Integ/GotuKola.html)

May also help normalize nail and hair growth.

According to Michael Moore, Centella can have a pituitary/hypothalamic “potentiating” and thyroid stimulating effect.

 

Photo: www.aridlands.com

 

Commiphora mukul (Guggul)-

Guggul is another herb used widely in Ayurveda; it is warming, anti-inflammatory, believed useful in cases of obesity, and cholesterol lowering.  As many cases of hypothyroidism can involve elevated cholesterol, the last effect may be particularly helpful in such cases. Guggul is specifically indicated for prevention of sluggish metabolism.  Studies have shown that once of its constituents, Z-guggulsterone, can increase the thyroid’s ability to uptake enzymes needed for effective hormone conversion.  It also increases oxygen uptake in muscles. (Shomon)

 

 

Lepidium meyenii (Maca Root)- Used successfully by indigenous peoples of Peru to help with hormonal imbalances, menstrual irregularities,fertility, and menopausal symptoms, including hot flashes, vaginal dryness, loss of energy, libido and depression. Its action relies on plant sterols, which act as chemical triggers to help the body itself produce a higher level of hormones appropriate to the age and gender of the person taking it. Clinical case studies have shown that maca can be effective for premenstrual syndrome (PMS), as well as menopausal symptoms, and may help symptoms of hypothyroidism as well.” http://www.thyroid-info.com/articles/macahrt.htm

Photo: www.rain-tree.com/maca-powder.htm

 

 

 

 

 

 

Photo: www.atlas-roslin.pl/…/Mahonia_aquifolium.htm

 

 

Mahonia aquifolium (Oregon Grape)-

The rhizome and root are used; constituents are alkaloids of isoquinoline type.  It is an alterative, cholagogue, laxative, antiemetic, anticatarrhal, and tonic.  Useful in chronic, scaly skin conditions. Tonic to liver and gallbladder. Useful as laxative in chronic constipation.  Tincture- 1-4 ml 3x/day or decoction 1-2 tsp root in 1 cup water. (DH)

Improves kidney and liver excretory function- which can be useful in keeping these organs clear of toxins and better able to process thyroid (and other hormones.)   May also be a mild thyroid stimulant. (RD)  It is blood building, stimulates glands of the body (particularly lymph and liver), and aids digestion; it can be helpful in diabetes and rheumatoid arthritis (which can sometimes be associated with hypothyroid.)  5-30 drops of tincture/fluid extract- the smaller effective dose, the better. (MW)

 

 

Avena Sativa (Oats)- Oats are a nervine tonic, antidepressant, nutritive, demulcent, and vulnerary.  The seed and whole plant are used; constituents are proteins, flavones, avenacosides, fixed oil, vitamin E, and starch.  Oats feed the nervous system when one is under stress; it’s specific for nervous debility and exhaustion associated with depression (both of which can be associated with hypothyroidism.) Dosage can be 3-5 ml 3x/day of tincture or one cup boiling water infused with 1-3 tsp. of straw 3x/day. (DH)  Can help with low libido and may be useful in lowering cholesterol.

Oats are tonic in cases of dryness and atrophy; this remedy has an  affinity for nerves (sympathetic excess), skin, hair, nails, and connective tissue.  It is useful when there is an inability to keep the fixed on one subject, a lack of focus and memory.  It can be helpful in insomnia associated with depression and nervous exhaustion.  (MW)

Photo: http://www.interhomeopathy.org/images/gallery/186-Avena-Sativa.jpg

 

 

Juglans nigra (Black Walnut)- hulls of walnut, leaves; It is VERY astringent, alterative, laxative, antibacterial, antiparasitic, (good for gallstones).  It acts on the thyroid- good for hypothyroid and high in iodine.  It is a traditional remedy for goiter in the south.  (Helpful in fibromyalgia, which can be associated with hypothyroid.) (MW)

 

Photo: www.botanic.cam.ac.uk/juglands.htm

 

 

Personal use: I have had positive results in my own use, as hypothyroid, of a combination of  Withania Somnifera, Centella Asiatica, Avena Sativa, and Mahonia aquifolium. Obviously any individual’s constitutional needs will vary, but as a side note, these four herbs could combine well to support a broad spectrum of hypothyroid related issues.  (However, Centella can be quite stimulating and may be too much for some people.)

 

Other herbs to consider for Hypothyroid:

The first three are sometimes part of TCM formulas for imbalances that may be seen as relating to a Western diagnosis of hypothyroidism.  Because TCM primarily uses formulas and has a very different understanding of this western defined pathology, it is hard to say for certain if these herbs would be applicable individually in such cases, but they are worth considering- and perhaps consulting a TCM practitioner for further information.

Astragalus membranaceus- Root is used; it is primarily an immunomodulator, as well as tonic (spleen, kidneys, lungs, and blood), stimulant, and diuretic.  Strengthens many functions of immune system, anti-cancer, hepatoprotective. (DH)  Note: Many cite it for use in hypothyroid, but others mention it for hyperthyroid- or even as contraindicated in hypothyroid.

Panax (Red Ginseng)- Root; adaptogen, tonic, stimulant, hypoglycemic. Very stimulating; good for general use in weak or elderly people.  Do not use in acute inflammatory condition or bronchitis.  (DH)  Can help build libido, as general builds energy level- both of which can be low in hypothyroid.

Polygonum multiflorum (He Sho Wu/ Fo ti)- Kidney and liver tonic, works on  symptoms associated with these deficiencies including insomnia, grey hair/hair loss, memory loss, lower back pain, low energy/libido, amongst others.  (contraindicated in cases of poor/damp digestion.)

 

Also: Crataegus spp. (Hawthorn), Cimicifuga racemosa (Black Cohosh), Ginkgo Biloba (Ginkgo), Allium sativum (Garlic), Medicago Sativa (Alfalfa), Serenoa repens (Saw palmetto), Rumex crispus (Yellow Dock), Coleus forskohlii, Triphala (Ayervedic formula), Schizandra chinensis, Anemone (Pulsatilla), Phytolacca (Poke root), Iris, *Oplopanax (Devil’s Club).

Note- Oplopanax was a traditional indigenous remedy on the west coast for symptoms resembling hyperthyroid.  For this reason, it is unclear if it would perhaps be contraindicated for hypothyroid (though perhaps its use was for an overall tonic effect on the gland, rather than thyroid cooling.)  In that vein, an herbalist that I spoke with recently has found much use for it in hypothyroid cases and has never seen any negative effects from it.

 

Herbs contraindicated in Hypothyroid:

It is important to be aware that some of the herbs that would be considered specific to hyperthyroid should be avoided for those with hypothyroid conditions, especially those herbs that have a definite thyroid suppressive action. The following list contains some herbs that fall into this category.

Melissa officinalis (Lemon Balm), Lycopus virginicus or europaeus (Bugleweed), Ocimum Sanctum (Holy Basil), Leonurus cardiaca (Motherwort), Trigonella foenum vulgare (Fenugreek) (unclear if it would be indicated for hyper, but said to have thyroid suppressive effects so to be avoid for people with hypo.)

 

Nutrition: Diet & Supplements

 

Diet is absolutely essential in the maintenance of thyroid health. Having an overall balanced food intake, based on whole, ideally organic, foods and drinking sufficient water is key to general health, and the thyroid is no exception.  However, specific foods can be thyroid suppressive or supportive.  Beginning with the former, soy comes up as a primary offender.  Soy contains high amounts of isoflavones, which are a member of the flavanoid family- a known category of endocrine disruptors.  These act as hormones, specifically phytoestrogens in the case of isoflavones, disrupting the normal activity and balance of natural hormones in the body.  Flavanoids are anti-thyroid agents; they inhibit thyroid peroxidase (TPO), an enzyme that frees up iodine for its use in the production of TH. (www.wikipedia.org)   While this can be particularly dangerous in soy based infant formulas,  overconsumption of soy in any form can cause significant problems.  For people with possible hypothyroid issues, it is probably best to avoid soy altogether.  Millet similarly has a high flavanoid content; hypothyroid is common in places where this grain is a dietary staple.  (M. Shomon, p. 269-270)

Cruciferous vegetables (broccoli, brussels sprouts, cauliflower, cabbage, rutabagas, turnips, kohlrabi, kale- and any other vegetables in the brassica family), particularly raw, are goitrogenic (thyroid suppressive) due to  their content of goitrin,  which impedes the body’s use of iodine.  (Langer and Scheer, p. 37)   There is some debate about whether cooking or fermenting these vegetables can decrease this effect.  It seems that these processes will likely cut down on the negative impacts, but it probably still wise to use moderation in cases of pre-existing hypothyroidism.

Other foods that should be avoided or reduced (for similar reasons) are:

Walnuts, peanuts, almonds, peaches, strawberries, cherries, apricots, prunes, garlic, lima beans, sweet potatoes, corn, and peas. (This list is not necessarily comprehensive.)

If they aren’t already being reduced for their other nasty effects, white sugar, white flour, caffeine, alcohol, and cigarettes should be cut down as they all have a negative impact on thyroid function.

As for thyroid stimulating/supportive foods, first: seaweed, seaweed, seaweed.  See the section above under herbs for more details (here we encounter the perennial line between herbs and food, and it should simply be acknowledged that herbs ARE food- and the exact classification varies on a cultural and individual basis.)  On his webpage, Ryan Drum offers a significantly longer discussion on the value of different species of seaweed and their exact nutritional content and recommended dosages.  Apparently garlic and root crops, such as turnips, carrots, potatoes, parsnips, sweet potatoes can contain some iodine, depending on the content in the soil in which they are grown; this can be increased greatly through fertilization with seaweed.  (R. Drum, “Thyroid Function and Dysfunction”, p. 5) (However- as seen above- others note garlic and sweet potatoes as potentially goitrogenic.)  Other sources of dietary iodine that may be appropriate for omnivores are red meat, seafood, eggs, and dairy. Some commercial baked goods may be due to their manufacture process.  Like a few seaweeds, red meat can also contribute to raising thyroid levels directly; in this case through globulin bound thyroid hormones in the animal’s blood.  Drum encourages consumption of the animal raw or as rare as possible (though I must admit that my vegetarian self cringes at writing this.)  (R. Drum, “Environmental Origins of Thyroid Dysfunction, p.4-5)

Hypothyroid individuals may benefit from certain supplements.  There are sometimes conflicting opinions on this topic, and again, not always adequate research to back a particular theory; but the following are some suggestions that may be worth incorporating to see for oneself if there is positive effect:

- L-tyrosine is a  precursor to thyroid hormone and low levels are sometimes found in conjunction with hypothyroidism, in which case supplementation may be of benefit. (Shomon, p. 123)

- Brewer’s/Nutritional Yeast can be an invaluable supplement of B vitamins (particularly B-12) and other nutrients, including selenium (depending on the brand).   This is particularly valuable to vegans/vegetarians who may not otherwise have ample sources of B-12.

- Overall B-complex vitamin- particularly B1 (Thiamin), B2 (Riboflavin), B3 (Niacin), B6 (Pyridoxine) , and B12 (Cobalamin).  B1 and B2 are connected to metabolism- B1 to carbohydrate metabolism and B2 to thyroid hormone metabolism specifically, catalyzing the  conversion of T4 to T3.  (Shomon, p. 124)  B3 assists cells in respiration and the metabolism of carbohydrates, fats, and proteins. B6 deficiency can lead to problems in the utilization of iodine to produce TH. B12 absorption is tied to proper thyroid function and it is not uncommon that an underactive thyroid can lead to malabsorption of this vital nutrient. (Langer and Scheer, p. 29-30.)

-Vitamin A- if the thyroid gland is underactive, there is not an efficient conversion of carotene (the source found in many foods- particularly vegetables) to usable vitamin A.  (Langer and Sheer, p. 26)

- Vitamin C deficiency can place strain on the thyroid (and in long term cases, even cause the thyroid cells to multiply at an abnormal rate and oversecrete- essentially ignoring signals from the pituitary.) (Langer and Scheer, p. 30)

- Vitamin E deficiency appears to also cause rapid thyroid cell multiplication, and also inadequate synthesis of TSH in the pituitary. (Langer and Scheer, p. 31)

Though both C and E deficiency seems to lead to conditions akin to hyperthyroidism, and thus would be indicated in such cases, adequate supply of these vitamins also helpful in hypothyroidism to promote overall healthy thyroid function.

- Selenium helps control the conversion of T4 to T3 by activating an essential enzyme. It seems that selenium also has a balancing effect in conjunction with iodine- too much iodine without adequate selenium can lead to thyroid damage. Stress and injury appear to decrease selenium levels and make the thyroid especially vulnerable. (Shomon, p. 172)  See Langer and Scheer 171-172 for a more in depth consideration. Selenium supplements are not recommended in women who are or are considering becoming pregnant. As excess selenium can be damaging, the dose in conjunction with adequate iodine should be carefully measured.

- Copper and Zinc can impact production of T4 and effect metabolism of TH in cells. It is critical that these two trace minerals be in balance within the body and that neither is excess nor deficient. (Langer and Scheer, p. 59)

- Essential fatty acids (EFAs) are critical for thyroid function. (Shomon, p. 123)  Evening primrose oil, particularly, can be useful.  Its essential fatty acids are precursors to prostaglandins, which are vital to all cells. They are critical to blood circulation, metabolism, growth and reproduction, and immune function.  (Langer and Scheer, p. 150.)  EFAs can be particularly supportive in hypothyroid, where the same body functions may not be carried out with maximum efficiency.

In most cases, supplement dosages are not included as they will vary based on an individual’s body size, age, and diet. It, therefore, seems most appropriate to research supplementation amounts on a case by case basis, using the above information as guideline for what nutrients might be called for.

 

 

Bibliography

(not including some specific URL’s which are cited in paper where appropriate):

 

Drum, Ryan. “Thyroid Function and Dysfunction,” “Environmental Origins of Thyroid

Disease- Part 1,” and “Environmental Origins of Thyroid Disease- Part 2.”

Available at http://www.ryandrum.com/.

Eng, Grace, M.D. – personal conversations

Fischer, Pam – class lectures.

Grieve, Maude.  A Modern Herbal. 1971 (1931), Dover Publications, New York, NY

Hoffman, David. Medical Herbalism. 2003, Healing Arts Press, Rochester, VT.

Kaptchuk, Ted J.  The Web That Has No Weaver. 2000, Contemporary Books, New

York, NY

Kopf, Eric, MD. “The Thyroid Gland.” Ohlone Center Lecture Paper, April 17, 2007.

Levoxyl_WebPl available at http://www.levoxyl.com/pi.asp.

Langer, Stephen E. and Scheer, James F.  Solved: The Riddle of Illness. 2000, Keats

Publishing. Lincolnwood, IL.

Mareib, Elain N. RN, PhD & Hoehn, Katja MD, PhD. Human Anatomy & Physiology;

Seventh Ad., 2007, Pearson Education, Inc. San Francisco, CA.

Moore, Michael. “Herbal Energetic in Clinical Practice”, Available at

http://www.swsbm.com

Muscat, Joshua – personal conversations

Shomon, Mary J. Living Well With Hypothyroidism. 2000, Avon Books, NY, NY;

(http://www.thyroid-info.com/index.htm)

University of Maryland Medical Center:

http://www.umm.edu/patiented/articles/what_causes_hypothyroidism_000038_2.htm

UpToDate site: http://www.utdol.com

Women to Women, http://www.womentowomen.com/hypothyroidism/

Wood, Matthew. The Practice of Traditional Western Herbalism. 2004, North Atlantic

Books, Berkeley, CA.