Thyroid Deficiency


The Thyroid Gland

The thyroid gland lies in the neck, just below the Adam's apple. It measures about 2 inches across and normally cannot be seen. It can barely be felt upon palpation. An enlarged thyroid, known as a goiter, can easily be detected by a physician upon examination. The thyroid gland secretes hormones which control the body's metabolic rate in two primary ways: by stimulating tissue response in the body to produce specialized proteins and by increasing cell oxygenation. To produce these vital hormones, the thyroid needs the element iodine, which is ingested from food and water.

The regulation of thyroid hormone levels is controlled by several mechanisms. The hypothalamus, located in the brain just above the pituitary gland, secretes thyrotropin-releasing hormone, which triggers the pituitary to release thyroid-stimulating hormone (TSH). When the amount of thyroid hormone in the blood reaches a certain level, the pituitary will produce less TSH; conversely, when the amount of thyroid hormone in the blood decreases to a certain level, the pituitary produces more TSH.

Thyroid Hormones

The thyroid gland secretes two significant hormones: thyroxine (T4) and triiodothyronine (T3). Approximately 93% of the hormone secreted by the thyroid is T4, with only 7% being T3.

In healthy people, almost all thyroxine is converted to triiodothyronine in the tissues. This means that the primary thyroid hormone finally delivered to and acting on tissues is T3. In normal health, maintenance of resting metabolism and excitability of membranes require between 35-50 mcg of T3 a day.

Thyroxine consists of two tyrosine molecules each binding two iodine constituents. The enzyme, 5-monodeiodinase, found in liver and in peripheral tissues, cleaves a single iodine from the outer tyrosine to create T3. Excess T4 is disposed of by action of a similar enzyme, which takes a single iodine from the inner tyrosine, and thus creates reverse T3, which is metabolically inactive.

Calcitonin (thyrocalcitonin) is another hormone secreted by the thyroid gland. Calcitonin maintains blood calcium levels by inhibiting bone breakdown and preventing excess calcium in the blood (hypercalcemia).


Because the thyroid stores a several weeks' supply of hormone, symptoms of deficiency may actually occur some time after the gland is damaged or compromised. Deficient production of thyroid hormone may reflect inadequate dietary iodine or autoimmune disease that attacks the glandular tissue.

In the absence of signs of frank thyroid disease, doctors often fail to properly assess thyroid function. Blood levels of TSH and T4 are helpful in some cases, but may be normal even in profound deficiency states.

The Achilles Tendon Reflex Recovery test and the Barnes Basal Temperature test may be helpful in disclosing cases of deficient conversion of T4 to T3. This is particularly important in evaluating systemic metabolic disorders such as obesity and metabolic diabetes. (The procedure for determining your basal temperature is given below in the text.)

Lowering the intake of calories (dieting) has the unfortunate consequence of diminishing production of T3, which in turn lowers the basal (resting) metabolic rate, which alone can lead to weight gain.

Thyroid Deficiency in Obesity and Diabetes
The enzyme that converts T4 to T3 is called 5-monodeiodinase. Unfortunately, this enzyme is inhibited in response to diminished caloric intake (dieting). That means that the fewer calories ingested, the lower the production of 5-monodeiodinase. This is the body's natural method of conserving fuel during shortage. Because "dieting" is not a natural state, it elicits the same physical reaction as famine--another reason why "eating less" will never effectively treat obesity. Deficient peripheral conversion of T4 to T3 is found almost universally in patients who become overweight.

The thyroid gland is located in the neck and measures about 2 inches across. Thyroxine (T4) and triiodothyronine (T3) stimulate energy metabolism in all the body's cells. Thyrocalcitonin, another thyroid hormone, regulates blood calcium levels by inhibiting bone breakdown. The parathyroid glands are located on the back of the thyroid gland. Parathyroid hormone (PTH) has the opposite effect of thyrocalcitonin. PTH increases blood calcium levels as needed by stimulating bone breakdown. (Anatomical Chart Company 2002?, Lippincott Williams & Wilkins)

Other Effects of Thyroid Deficiency
A thyroid deficiency (hypothyroidism) means that the thyroid gland is producing too little thyroid hormone. The symptoms of hypothyroidism are gradual and are sometimes mistaken for depression. Facial expressions become dull, the voice becomes hoarse, eyelids droop, and the face and eyes become puffy and swollen.

Hypothyroidism can cause a number of other conditions, such as allergies, skin problems, fatigue, nervousness, gaining or losing weight, brittle nails, dry skin, gastrointestinal problems (constipation), infertility, mental sluggishness, low immune function, depression, and intolerance to cold. Carpal tunnel syndrome has also been associated with thyroid deficiency.

The thyroid gland is located in the neck and measures about 2 inches across. Thyroxine (T4) and triiodothyonine (T3) stimulate energy metabolism in all the body's cells. Thyrocalcitonin, another thyroid hormone, regulates blood calcium levels by inhibiting bone breakdown. The parathyroid glands are located on the back of the thyroid gland. Parathyroid hormone (PTH) has the opposite effect of thyrocalcitonin. PTH increases blood calcium levels as needed by stimulating bone breakdown. (Anatomical Chart Company 2002?, Lippincott Williams & Wilkins)

If left untreated, hypothyroidism can cause anemia, low body temperature, and heart failure. A life-threatening condition known as myxedema coma may ensue in which respiration slows, seizures occur, and blood flow to the brain decreases. Exposure to cold, infections, tranquilizing drugs, and trauma can trigger myxedema coma.

There is some evidence that low T3 levels may be associated with breast cancer. A study in Molecular Carcinogenesis (Gonzalez-Sancho et al. 2002) stated that T3 down-regulated the expression of T1, a gene that is over-expressed in human breast adenocarcinomas. The study concluded that T3 reduced the proliferation of mammary epithelial cells and inhibited the expression of cyclin D1 and T1 genes. Another study in the Annals of Medicine (Smyth 1997) indicated that although the exact mechanism for the association between thyroid and breast cancer is not quite clear, there is the possibility that the presence of thyroid abnormalities may influence breast cancer progression, and this should stimulate awareness into the coincidence of the two disorders. Finally, according to the World Health Organization, 45.5% of patients with a breast carcinoma had thyroid enlargement compared with only 10.5% of controls. Antithyroid peroxidase autoantibodies were twice as common in breast cancer patients as in controls. These findings provide evidence of a relationship between thyroid disease and breast carcinoma, although the mechanisms require further study (Shering et al. 1996).


Thyroid deficiency generally affects women who are over the age of 40, but it can also affect men and teenagers, especially if it runs in the family. The elderly are particularly susceptible to undiagnosed or subclinical hypothyroidism. Hypothyroidism is also associated with pernicious anemia (vitamin B12 deficiency) and insulin-dependent diabetes.


Hashimoto's thyroiditis is the most common form of hypothyroidism, presenting with an enlarged thyroid gland that becomes nonfunctional, with the active parts of the gland deteriorating after several years. Hashimoto's thyroiditis is a chronic inflammation of the thyroid gland thought to be caused by autoimmune factors. Other forms of autoimmune disease are common, including pernicious anemia, rheumatoid arthritis, systemic lupus erythematosus (SLE), and Sj?gren's syndrome. Schmidt's syndrome refers to hypothyroidism with other endocrine disorders, including Addison's disease (adrenal insufficiency), hypoparathyroidism, and diabetes mellitus, all of which may be autoimmune in nature.

Euthyroid sick syndrome is hypothyroidism, associated with a severe systemic illness, that causes decreased peripheral conversion of T4 to T3, an increased conversion of T3 to the inactive reverse T3, and decreased binding of thyroid hormones. Conditions commonly associated with this syndrome include fasting, starvation, protein-calorie malnutrition, general surgical trauma, myocardial infarction, chronic renal failure, diabetic ketoacidosis, anorexia nervosa, cirrhosis, thermal injury, and sepsis. Once the underlying cause is treated, the condition is usually resolved.

Treatment for hyperthyroidism, which includes administering radioactive iodine and surgical removal of the thyroid gland, may also result in hypothyroidism.

In many undeveloped countries, where there is a chronic lack of iodine in the diet, goitrous hypothyroidism resulting from an underactive thyroid gland is common. Hypothyroidism resulting from a lack of dietary iodine has disappeared in the United States.

Drugs that may produce hypothyroidism as an adverse reaction include amiodarone (Cordarone), colchicine (Colsalide), fluoxetine (Prozac), interferon-alfa (Alferon N, Intron A, Roferon A), lithium (Eskalith, Lithobid), methimazole (Tapazole), potassium iodide, KI (Pima, SSKI), and propylthiouracil.

Risk Factors

Smoking has also been identified as a risk factor for hypothyroidism, but the reason for the association is unknown (Nystrom et al. 1993).

Hypothyroidism may also be caused by occupational exposure to lead (Lasisz et al. 1992).

A recent study measured the plasma homocysteine levels in 50 hypothyroid and 46 hyperthyroid patients. They found that plasma homocysteine concentrations increased in hypothyroidism and decreased in hyperthyroidism. They also found that restoration of the euthyroid state (by drug treatment) decreased both homocysteine and creatinine in hypothyroid patients and increased both homocysteine and creatinine in hyperthyroid patients. Folate levels were found to be lower in the hypothyroid group when compared with the hyperthyroid group. They proposed that a higher creatinine clearance in hyperthyroidism could partially explain the changes in homocysteine. A similar study found the same relationship between homocysteine and hypothyroidism, but the authors believed it was due to decreased hepatic levels of enzymes involved in the remethylation pathway of homocysteine (Nedrebo et al. 1998; Hussein 1999; Catargi et al. 1999; Diekman et al. 2001).


Overt hypothyroidism is easy to diagnose by a simple blood test. Low levels of T3 and T4 are signs that you do not have enough thyroid hormones. An elevated TSH is a sign of thyroid deficiency. When your TSH is high, it means the pituitary gland is trying to make the thyroid gland produce more hormones. Patients with euthyroid sick syndrome, however, have a normal TSH.

Hashimoto's thyroiditis is diagnosed by high titers of antithyroid (antimicrosomal) antibodies. High titers of antibody against thyroglobulin (TG) and thyroid peroxidase (TPO) are present in most patients.

If, however, someone is suffering from the classic symptoms of thyroid deficiency but has normal test results, the thyroid slowdown could be slight or age- related and is not easily detected by a blood test. Thyroid deficiency often mimics many symptoms associated with old age. One way to determine a thyroid deficiency is to have your physician test for a substance called transthyretrin (also known as prealbumin). Thyroid hormone is carried through the bloodstream and brain by transthyretrin. Even when all other hormones are normal, a low level of trans-thyretrin could mean that you are not producing enough thyroid hormones and that it is not being delivered to the cells.

Another sensitive laboratory test to measure thyroid deficiency is the TRH (thyrotropin-releasing hormone) stimulation test. It can show whether a patient is suffering from an underactive thyroid even when routine thyroid tests reveal nothing. The patient's level of TSH is measured through a blood test, then the patient is given an injection of TRH (a harmless synthetic hormone, modeled after the TRH secreted by the hypothalamus gland in the brain); 25 minutes later blood is drawn and the TSH is measured again. If the measures from the second TSH blood test are high (above 15), then the patient's thyroid is underactive.

The TRH injection stimulates the brain's pituitary gland, which produces TSH and regulates the thyroid. If the thyroid is under-functioning, the pituitary gland will secrete excess TSH.

Barnes Basal Temperature Test
Another way of detecting a possible thyroid deficiency is to take your basal body temperature. Place a thermometer at your bedside, and as soon as you wake up before you step out of bed, place the thermometer under your arm for at least 3 minutes. If you are T3 deficient, you will find your basal temperature to be below 97.8F (normal throughout the day is 98.6F). If your first-thing-in-the-morning temperature is consistently low, it likely means that your basal (resting) metabolic rate is also low.

Record the time, date, and temperature every morning for 2 weeks to show your doctor. In addition to following up with blood tests, your doctor can determine the patency of your deep tendon reflexes, especially the time it takes your Achilles tendon to recover after first elicitation.


Conventional treatment calls for the oral replacement of deficient thyroid hormones. A synthetic form of T4 (Synthroid, Levothroid, Levothyroxine) is most often administered. Treatment, especially in older people, begins with low doses of thyroid hormone because serious side effects may occur with too large a dose. The dose is gradually increased until TSH levels in the blood return to normal. The medication must usually be taken for life.

Synthroid is the third most popular drug prescribed in the United States, being taken by 8 million people. The drug was introduced in 1955 without FDA approval. Recently the safety, stability, and efficacy of this drug have come under fire. In April 2001 the FDA denied Abbott Laboratory's request that Synthroid be allowed to bypass a new drug application and be declared "generally recognized as safe and effective." Instead the FDA stated that Synthroid "had a history of problems with potency and stability" and required Abbott to file the necessary application and study results by August 14, 2001, for official review and approval. Final review and approval was granted by the FDA in July 2002. A condition of approval was that Abbott is required to "develop an analytical method for the determination of impurities and degradation products in the drug substance and the drug product" by July 31, 2003.

Several studies have questioned the effectiveness of levothyroxine and other synthetic T4 drugs for various treatments of thyroid disorders. One study evaluating its ability to suppress the number of nodules in patients with multinodular euthyroid goiter showed limited effectiveness in reduction of nodules. This study also indicated it was ineffective for body weight reduction in obese patients (Imbrogno et al. 2001).

For some patients, hypothyroidism symptoms persist despite standard thyroxine replacement therapy. Thyroxine therapy was no more effective than placebo in improving cognitive function and psychological well-being in patients with symptoms of hypothyroidism, despite thyroid function tests falling well within the reference range (Pollock et al. 2001; Walsh et al. 2001).

Unithroid (levothyroxine), previously known as Thyrox, was approved by the FDA on August 22, 2000, as the first FDA-approved levothyroxine (synthetic T4) drug on the market. Many physicians are recommending that their patients switch from other non-FDA-approved drugs (such as Synthroid) to Unithroid.

On May 25, 2001, Levoxyl received FDA approval as the second levothyroxine drug. Many patients prefer Levoxyl because of its lower price.


Armour Thyroid
Armour thyroid (Thyrar), Nathroid, and Westhroid are prescription medications that contain desiccated thyroid derived from the thyroid gland of the pig. Natural thyroid extracts have been used since 1892 and were approved by the FDA in 1939. Armour thyroid and most other natural glandular preparations are made to standards approved by the United States Pharmacopoeia (U.S.P.), which ensures that its potency is accurately stated on the label.

Natural thyroid extracts were largely replaced in clinical medicine by levothyroxine (Synthroid). Most physicians are reluctant to prescribe natural glandulars because they are told that they are impure and inconsistent from dose to dose. If your physician requires more information on natural glandulars, contact the Broda O. Barnes Research Foundation listed in the summary.

An article in the New England Journal of Medicine described a study in which patients with hypothyroidism showed greater improvements in mood and brain function if they received treatment with Armour thyroid rather than Synthroid (thyroxine). The authors also detected biochemical evidence that thyroid hormone action was greater after treatment with Armour thyroid. The patients who were on Armour thyroid had significantly higher serum concentrations of sex hormone-binding globulin; having higher concentrations of sex hormone-binding globulin is not a favorable event (Bunevicius et al. 1999).

Liothyronine (Cytomel, Triostat) is a synthetic form of T3 that was approved by the FDA in 1954. It is preferred over Synthroid (synthetic T4) by many doctors because it does not require conversion in the body (T4 must be converted to T3, the metabolically active form). For this reason, the Life Extension Foundation recommends Cytomel instead of synthetic T4 medication.

The standard dose of Cytomel is 25 mcg orally once daily, increasing by 12.5 mcg every 1-2 weeks if required. Approximately 15-37.5 mcg of Cytomel is equal to 60 mg of desiccated thyroid.

An article in the New England Journal of Medicine reports on the results of research comparing the effects of thyroxine alone with those of thyroxine plus triiodothyronine (Cytomel) in 33 patients with hypothyroidism. The combination group scored higher on six of the 17 tests of cognitive performance and assessments of mood. The authors stated: "Treatment with thyroxine plus triiodothyronine improved the quality of life for most patients" (Bunevicius et al. 1999). Gupta et al. (2001) showed a link between low serum T3 levels and patient mortality in elderly hospitalized patients.

Liotrix (Thyrolar) is a mixture of synthetic T4 and T3 in a 4:1 ratio by weight used to treat hypothyroidism. The standard dose is initially 30 mg orally perday, with an increased dose every 2-3 weeks if clinical response indicates. Most patients will require 60-120 mg perday. Approximately 60 mg of Thyrolar is equal to 60 mg of desiccated thyroid.


Because the various thyroid drugs have similar actions, the side effects, contraindications, and drug interactions are almost identical for each.

Adverse reactions to thyroid medications include many of the signs of hyperthyroidism, including:

Thyroid medications interact with several classes of medications:

Thyroid medications are contraindicated in:

Absorption of thyroid medications is impaired by:


Natural supplements for thyroid problems include vitamin A; vitamin B complex; B12; and the vitamins C, and E; as well as coenzyme Q10; and especially the minerals magnesium, manganese, selenium, and zinc, all of which can be found in ample amounts in the Life Extension Mix. Deficiencies of any of these minerals can prevent the conversion of T4 to T3 and should be corrected. Sufficient protein iodine and especially the amino acid tyrosine are necessary to make T4 in the thyroid gland.

Treatment of autoimmune hypothyroidism (Hashimoto's) and euthyroid sick syndrome is based upon the underlying disorder (refer to the Autoimmune, Arthritis, and other relevant protocols for more information).

Thyroid hormones are made by adding iodine molecules. Hence, a dietary deficiency of iodine can be a cause of hypothyroidism. Iodine is found in kelp and other seaweeds and seafood. It is also available in iodized salt. Those who suffer from autoimmune thyroid disease, such as Hashimoto's thyroiditis or Graves' disease, may want to avoid taking extra iodine because this disorder is not due to iodine deficiency and will not be of much help. For some it may irritate the thyroid and make matters worse.

Tyrosine is a precursor of thyroid hormone and the neurotransmitters dopamine, norepinephrine, and epinephrine. A deficiency of tyrosine leads to hypothyroidism and low adrenal function. The recommended daily amount of tyrosine is about 1 gram perday for adults (Marz 1997).

Selenium assists in removing toxins from the body through the enzyme glutathione peroxidase. Selenium is readily available in many foods, such as asparagus, grains, garlic, and mushrooms. Many agricultural areas, however, are extremely deficient in selenium. Research has linked selenium with thyroid function. One study found that the combination of both iodine and selenium deficiency was particularly toxic to the thyroid gland (Contempre et al. 1995).

A recent study in Belgium used selenium (20-60 mcg perday) to treat 18 children with congenital hypothyroidism. Supplementation with selenium caused a 74% increase in plasma selenium and normalized the levels of TSH. The authors concluded that selenium improves the thyroid hormone feedback system and improves the conversion of T4 to active T3 (Chanoine et al. 2001).

Another article described the use of selenium in three cases of hypothyroidism in children. After only 4 weeks of supplementation, they saw a marked improvement of all clinical symptoms and a return to normal metabolism (Pizzulli et al. 2000).

A double-blind, placebo-controlled study of 36 elderly subjects conducted in Italy found a linear correlation between selenium levels and T4 (as well as the ratio of T3:T4). Reduced conversion of T4 to T3 causes an overt hypothyroid condition that is common in the elderly. The main result of the study was a significant improvement in selenium levels and a decrease in the T4 levels in selenium-treated subjects (Olivieri et al. 1995).

Dehydroepiandrosterone (DHEA)
DHEA, a hormone that enhances the body's metabolic functioning, may also be deficient in individuals with hypothyroidism (Tagawa et al. 2000). A DHEA blood test should be administered to achieve optimal dosing (see the DHEA-Pregnenolone Precautions in the DHEA Replacement Therapy protocol for more detailed information).

Thyroid & L-Tyrosine Complex
Thyroid & L-Tyrosine Complex by Enzymatic Therapy combines thyroid tissue, the amino acid tyrosine, and synergistic trace minerals that must be present for endocrine gland functions, especially the thyroid. The thyroid gland needs iodine and L-tyrosine to produce hormones that control the body's metabolism. The trace minerals manganese, zinc, copper, and molybdenum included in the formula are involved with specific enzymes linked to endocrine glandular processes.

The effect of soy on thyroid function is currently a controversial topic. Some believe that soy increases metabolic rate and thyroid function. Several recent articles, however, have noted problems with people taking soy supplements.

One study identified the mechanism of soy's effect on thyroid function. Genistein and daidzein, the isoflavones in soy, inhibited thyroid peroxidase by acting as alternative substrates (Divi et al. 1997).

Soy-based infant formulas have been associated with an increased incidence of autoimmune thyroid disease and diabetes when compared with breast-fed infants (Fort et al. 1986; Fort et al. 1990).

Soy supplements should be avoided by hypothyroid patients because they increase the amount of thyroxine needed to attain clinical effect (Bell et al. 2001; Jabbar et al. 2001).


Some foods contain goitrogenic substances that prevent the utilization of iodine. Goitrogens are found in sweet potato, cabbage, cauliflower, turnips, rutabaga, rapeseed oil (canola), cassava, pine nuts, mustard, millet, soybeans, and peanuts. The actual content of goitrogens in these foods, however, is quite low, and cooking inactivates them.


How to best diagnose thyroid deficiency has been a long-standing medical controversy. Conventional doctors rely on thyroid blood tests, whereas alternative physicians look for signs and symptoms of thyroid deficiency. An article in The Lancet revealed surprising findings about reference ranges that may alter the way physicians assess individual thyroid status.

Before The Lancet article is discussed, the reader should be reminded of the serious consequences of a thyroid hormone deficiency. Aging people encounter a variety of ailments that doctors often attribute to problems other than thyroid deficiency. Some of the most noticeable symptoms caused by low thyroid are poor concentration, memory disturbances, cold hands and feet, accumulation of excess body fat, difficulty in losing weight, menstrual problems, dry skin, thin hair, and low energy levels. Some specific disorders related to thyroid deficiency include depression, elevated cholesterol, migraine headaches, hypertension, and infertility (Stanosz 1992; Saito et al. 1994; Vierhapper 1997; Michalopoulou et al. 1998; Pop et al. 1998; Lincoln et al. 1999; Krassas 2000; Hagen et al. 2001; Spierings 2001).

Broda O. Barnes was a physician-scientist who dedicated more than 50 years of his life to researching, teaching about, and treating thyroid and related endocrine dysfunctions. In his book entitled Hypothyroidism: The Unsuspected Illness, Dr. Barnes described more than 47 symptoms that may be related to poor thyroid function. During his many years of research and practice, Dr. Barnes condemned conventional doctors who ignored obvious clinical manifestations of thyroid deficiency. According to Dr. Barnes: "The development and use of thyroid function blood tests left many patients with clinical symptoms of hypothyroidism undiagnosed and untreated."

In lieu of blood tests, Dr. Barnes advocated that patients measure their temperature upon awakening. If the temperature is consistently below normal ranges, this is indicative of a thyroid deficiency. The Barnes Basal Temperature test, which appears earlier in this protocol, provides specific instructions on how best to measure your body temperature in order to assess thyroid hormone status.

Dr. Barnes believed that 40% of the adult population suffered from thyroid deficiency. Based on the percentage of adults now taking prescription drugs to treat depression, elevated cholesterol, and high blood pressure, Dr. Barnes' observations about the epidemic of thyroid deficiency may now have been validated.

The Lancet is one of the most prestigious scientific journals in the world. It often reports new medical findings that defy conventional wisdom. According to the August 3, 2002, issue of The Lancet, the problem with thyroid blood tests may be caused by inadequate laboratory reference ranges that fail to reflect what the optimal level of thyroid hormone should be in a particular individual (Dayan et al. 2002).

The Life Extension Foundation has discussed the issue of faulty laboratory reference ranges for many years. The problem is that for many blood tests, the laboratories provide a wide range that represents "average" populations, rather than what the optimal level should be to maintain good health.

Back in the 1960s, for instance, the upper reference range for cholesterol extended up to 300 (mg/dL). This number was based on a statistical calculation indicating that it was "normal" to have total cholesterol levels as high as 300. At that time, it was also "normal" for men to suffer fatal heart attacks at relatively young ages. As greater knowledge accumulated about the risk of heart attack and high cholesterol, the upper limit of the reference range gradually dropped to the point where it is now 200 (mg/dL) (ADVANCEDATA).

The same situation occurred with homocysteine reference ranges. Up until recently, it was considered normal to have a homocysteine blood reading as high as 15 (mcmoles/L) (Mahanonda et al. 2001). Most reference ranges now provide a chart showing that homocysteine levels above 7 increase risk of heart attack and stroke (Robinson et al. 1995).

It is not just blood laboratory reference ranges that fail to provide physicians and patients with optimal numbers. For example, when your blood pressure is checked, a diastolic number up to 90 (mmHg) is considered normal. Yet a diastolic blood pressure reading greater than 85 is associated with an increased stroke risk. A high percentage of people over age 60 have diastolic readings greater than 85, and this is the age group most vulnerable to stroke (Hansson et al. 1998). So when your doctor checks your blood pressure and says it is normal, your response should be that "normal" is not good enough because it is also normal for people over age 60 to suffer a stroke. Instead, you should ask your doctor what is the "optimal" range. In the case of diastolic blood pressure, taking steps to keep it at 85 or below could greatly reduce long-term vascular damage. It is important to note that midlife hypertension predisposes people to stroke later in life, so keeping blood pressure readings in optimal ranges is important at any age.

Scientists are now examining epidemiological data related to thyroid hormone reference ranges, and their findings indicate that it may be time to change the way laboratories report their TSH results.


The standard blood test used to determine thyroid gland hormone output is the TSH test. When there is a deficiency in thyroid hormone, the pituitary gland releases more TSH to signal the thyroid gland to produce more hormones.

When the TSH test is in normal range, doctors usually assume that the thyroid gland is secreting enough thyroid hormone. The question raised by The Lancet authors, however, is whether today's reference range for TSH reflects optimal thyroid hormone status.

The TSH reference range used by many laboratories is between 0.2-5.5 (mU/L). A greater TSH number is indicative of a thyroid hormone deficiency. That is because the pituitary is over-releasing TSH based on lack of thyroid hormone in the blood. Any reading more than 5.5 alerts a doctor to a thyroid gland problem and that thyroid hormone therapy may be warranted.

The trouble is that the TSH reference range is so broad that most doctors will look at a TSH reading as low as 0.2 and think it is as normal as a 5.5 reading. The difference between 0.2-5.5, however, is an astounding 27-fold. It would seem almost absurd to think that a person could be in an optimal state of thyroid health anywhere along this 27-fold parameter, that is, TSH readings between 0.2-5.5.

A review of published findings about TSH levels reveals that readings of more than 2.0 may be indicative of adverse health problems related to insufficient thyroid hormone output. One study showed that individuals with TSH values of more than 2.0 have an increased risk of developing overt hypothyroid disease over the next 20 years (Vanderpump et al. 1995). Other studies show that TSH values greater than 1.9 indicate abnormal pathologies of the thyroid, specifically autoimmune attacks on the thyroid gland itself that can result in significant impairment (Hak et al. 2000).

More ominous was a study s14howing that TSH values of more than 4.0 increase the prevalence of heart disease, after correcting for other known risk factors (Hak et al. 2000). Another study showed that administration of thyroid hormone lowered cholesterol in patients with TSH ranges of 2.0-4.0, but had no effect in lowering cholesterol in patients whose TSH range was between 0.2-1.9 (Michalopoulou et al. 1998). This study indicates that in people with elevated cholesterol, TSH values of more than 1.9 could indicate that a thyroid deficiency is the culprit causing excess production of cholesterol, whereas TSH levels below 2.0 would indicate no deficiency in thyroid hormone status.

Doctors routinely prescribe cholesterol-lowering drugs to patients without properly evaluating their thyroid status. Based on the evidence presented to date, it might make sense for doctors to first attempt to correct a thyroid deficiency (based on a TSH value over 1.9) instead of first resorting to cholesterol-lowering drugs.

In a study to evaluate psychological well-being, impairment was found in patients with thyroid abnormalities who were nonetheless within "normal" TSH reference ranges (Pollock et al. 2001).

Defying the Reference Ranges
The authors of The Lancet study stated that "the emerging epidemiological data begin to suggest that TSH concentrations above 2.0 (mU/L) may be associated with adverse effects." The authors prepared a chart based on previously published studies that provide guidance when interpreting the results from TSH blood tests. Here are three highlights from their chart that may be useful in ascertaining what your TSH values really mean:

  1. TSH greater than 2.0: Increased 20-year risk of hypothyroidism and increased risk of thyroid autoimmune disease (Vanderpump et al. 1995)
  2. TSH greater than 4.0: Greater risk of heart disease (Hak et al. 2000)
  3. TSH between 2.0-4.0: Cholesterol levels decline in response to thyroxine (T4) therapy (Michalopoulou et al. 1998)

Despite presenting these intriguing findings, The Lancet authors stated that more studies were needed to define optimal TSH level as between 0.2-2.0 instead of between 0.2-5.5. For a health-conscious person, however, this type of precise information provides an opportunity to correct a medical condition that has been unresponsive to mainstream therapies or possibly to prevent disorders from developing in the first place.

This means if you have depression, heart disease, high cholesterol, chronic fatigue, poor mental performance, or any of the many other symptoms associated with thyroid deficiency, you may want to ask your doctor to "defy the reference ranges" and try different thyroid replacement therapeutic approaches.

Measuring Thyroid Hormone Levels
TSH is just one blood test that doctors use to assess thyroid status. Other blood tests measure the actual amount of thyroid hormone found in the blood.

The primary hormone secreted by the thyroid gland is called thyroxine (T4). The T4 is then converted in the peripheral tissues into metabolically active triiodo-thyronine (T3). Doctors often test for TSH and T4 together, but this may not accurately reflect thyroid deficiency in tissues throughout the body. One study found that psychological well-being could be improved if T3 (e.g., the drug Cytomel) were added to T4 (e.g., the drug Synthroid) therapy, while maintaining thyroid function broadly within the standard reference ranges (Bunevicius et al. 1999; Walsh et al. 2001). What this means is that even when TSH and T4 blood tests are within normal ranges, a person can still be deficient in peripheral T3 and benefit from Cytomel therapy.

Because T3 is the metabolically active form of thyroid hormone, some physicians use it exclusively in lieu of T4 drugs like Synthroid. The FDA's recent notice to ban synthetic T4 drugs like Synthroid because of inconsistent potencies helps to validate a statement made by Broda Barnes more than 50 years ago: "Patients taking thyroid replacement therapy have much better improvement of symptoms with natural desiccated thyroid hormone rather than synthetic thyroid hormones."

Although the FDA has found many problems in T4 drugs, the T3 drug Cytomel has produced consistent clinical results and is not a subject of the FDA's proposed ban. Dr. Barnes fought the drug companies against synthetic T4 drugs for years and recommended desiccated thyroid (Armour) drugs as the therapy of choice for most patients.

An article in the New England Journal of Medicine described a study in which patients with hypothyroidism showed greater improvements in mood and brain function if they received treatment with Armour thyroid rather than Synthroid (thyroxine). The authors also detected biochemical evidence that thyroid hormone action was greater after treatment with Armour thyroid (Toft 1999).

Thyroid deficiency occurs when the thyroid gland under-produces the hormones thyroxine (T4) and triiodothyronine (T3) needed to regulate the body's metabolic rate. In some individuals, the thyroid does not properly convert T4 to T3, the metabolically active form. Supplementation with synthetic or animal-derived thyroid hormone is necessary to return hormone levels to normal.

Synthetic hormone supplementation, prescribed by a physician, includes synthetic T4 (Synthroid, Unithroid, and Levoxyl), synthetic T3 (Cytomel), and a combination of synthetic T3 and T4 (Thyrolar).

Natural glandulars (by prescription), such as Armour Desiccated Thyroid Hormone, Nathroid, and Westhroid, derived from the thyroid gland of the pig, contain T4 and T3, and most closely resemble natural human thyroid hormone.

Suggested supplements and their dosages follow:

  1. Iodine, 1 mg perday
  2. Selenium, 200-600 mcg perday
  3. Tyrosine, 500-1000 mg perday
  4. Melatonin, 300 mcg-6 mg at bedtime
  5. DHEA, 25 mg 1-3 times perday (refer to DHEA Replacement Therapy protocol)
  6. CoQ10, 100-200 mg daily
  7. Life Extension Mix for vitamin A, vitamin B complex, magnesium, manganese, selenium, and zinc, to be taken as directed
  8. Thyroid & L-Tyrosine Complex, 2 capsules 3 times daily


Contact the Thyroid Foundation of America, (800) 832-8321. For more information on natural glandulars or the basal body temperature test, contact the Broda O. Barnes, M.D. Research Foundation, P.O. Box 98, Trembly, CT 06611, (203) 261-2101.


Life Extension Mix, Coenzyme Q10, selenium, melatonin, L-tyrosine, and Thyroid & L-Tyrosine Complex by Enzymatic Therapy are available by calling (800) 544-4440 or by ordering online.