The thyroid gland secretes hormones that regulate critical metabolic functions. The two main thyroid hormones are thyroxine (T4) and triiodothyronine (T3). These hormones regulate body temperature, metabolism, energy, cholesterol, weight, and cognitive function. As we age, thyroid hormone production can decline, cuasing a condition known as hypothyroidism. Thyroid is the only hormone that affects virtually every cell in the body; thus, there are dozens of symptoms related to hypothyroidism, including hair loss, fatigue, weight gain, depression, poor circulation, dry skin, hair, and nails, and emotional instability. If you have asked your doctor to check your thyroid and were told “your levels are normal,” yet you still have symptoms of hypothyroidism, you are not alone. Although mainstream medicine has been slow to acknowledge it, there are now a great many studies showing that there is a significant difference between levels that are technically within the normal range, and levels that are optimal for your health and well-being. Restoring optimal thyroid function can significantly increase energy, metabolism and mood as well as decrease the risk of heart disease.
- Maintain weight and energy
- Improve concentration and mood
- Aid cellular growth and metabolic function
See the THYROID STUDIES section to review those studies now, or read on for more detailed Thyroid information:
The thyroid gland produces four hormones. The two main thyroid hormones are thyroxine (also called T4 because it contains four iodine atoms) and triiodothyronine (T3, containing three iodine atoms).
Most prescriptions for hypothyroidism replace only one thyroid hormone: Thyroxine (T4). The generic name for thyroxine is levothyroxine; it is sold as Synthroid, Eltroxin, Levoxyl and others.
What about the other three thyroid hormones? Why aren’t those replaced? How many do we need?
T4 is a slow-acting pre-hormone: it actually has no effect in the body until it is converted to T3. Ingested T4 takes four days to peak in the blood, and the overall effects aren’t reached for about six weeks. This slow, steady action is part of why most doctors prefer to prescribe it alone instead of with T3. Ingested T3 is faster acting, and its effects last for one to two days.
The thyroid hormones travel through the bloodstream to every cell in the body, where they keep everything working optimally, like oil in an engine. Without enough thyroid hormone in its active state (T3), the metabolism slows down, resulting in lowered pulse rate, coldness, weight gain, and fatigue. Other body functions slow down as well — the mind can’t function normally, skin becomes dry and flaky, hair falls out, muscles become cramped, and so on.
Additional hormones your thyroid makes are T1 and T2. Much less is known about T1 and T2. In medication form, they are found only in dessicated thyroid (Armour Thyroid, Westhroid and others). Dessicated thyroid is natural thyroid hormone derived from pigs’ thyroids; it was the main treatment for hypothyroidism from about 1895 until 1960 when Synthroid (Synthetic Thyroid) came out. Dessicated thyroid was known as a very safe and effective treatment.
Many thyroid patients do quite well on T4 medication alone, or on T4 and T3 together. However, for those that don’t, desiccated thyroid is a good option. The majority of patients who switch to desiccated thyroid find that their health improves, so these unmeasured hormones (T1 and T2) appear to have some function.
About 20 percent of the body’s T3 comes from the synthesis of T3 within the thyroid. The rest of the T3 is derived when an enzyme (called a deiodinase) removes one iodine molecule from T4. While T4 is converted to T3 in a number of locations in the body, the main place that this occurs is in the liver.
All the thyroid hormone metabolic activity comes from T3. Except during pregnancy, when T4 is needed for the fetus to develop properly, T4 is in the body just to be converted to T3. In a normally-functioning thyroid, enough of this conversion process takes place. Most people with hypothyroidism do not have normally-functioning thyroids, however. If you give those patients T4-only medication, many of them may not be able to able to convert that T4 adequately into T3. This is one reason why levothyroxine does not always make patients feel better.
This isn’t a problem for everyone with hypothyroidism, but lab test results sometimes don’t indicate a conversion problem when there is one. Most doctors are trained to check only T4 and TSH levels, and therefore are unaware of the Free T3 level, which is a useful measure of how much metabolically active T3 is available to the patient. The majority of those on T4 alone who still have symptoms of hypothyroidism benefit from taking T3 in a natural or synthetic form, usually in addition to T4.
The pituitary is an endocrine gland located at the base of the brain. It is exquisitely sensitive to the thyroid hormone levels in the blood. TSH (thyroid stimulating hormone), a pituitary hormone, stimulates all aspects of thyroid function from synthesizing thyroid hormones to releasing them into the bloodstream. When the thyroid hormone level drops, the pituitary releases more TSH. The thyroid releases more T4 and T3 into the bloodstream in response. As the thyroid hormone levels rise, the pituitary reduces or shuts off TSH. This feedback mechanism keeps the level of thyroid hormones in a fairly constant range– assuming a normally-functioning thyroid.
A high TSH level should indicate low thyroid hormone levels, and a low TSH level should indicate optimal or high thyroid hormone levels. However, although TSH is part of the endocrine system, it is not a thyroid hormone. Precisely what TSH level indicates in each person’s body that it isn’t getting enough thyroid hormone? What if the thyroid is producing enough T4, but the body isn’t converting enough of that T4 to T3? Why assume that the pituitary and the hypothalamus, which controls the pituitary, are functioning optimally when another part of the endocrine system isn’t? If they’re malfunctioning, the feedback mechanism can’t work.
Around 1974, the medical establishment decided that the TSH test was the test to diagnose hypothyroidism and hyperthyroidism, and to determine the amount of medication needed. In fact, diagnosing according to symptoms (how the patient feels) was put aside in favor of getting the diagnosis from a blood test. This was apparently done without any testing to see if TSH lab test results correlated with symptoms.
The main problem with the TSH test is that the reference range for it is too wide at most labs. The upper end of the range at many labs is as high as 5, but in reality, symptoms of hypothyroidism accompanied by a TSH level over 2 are good reason to suspect hypothyroidism. Overreliance on the TSH level is one reason why so many women are told their thyroid tests are “normal” even though they feel many classic symptoms of hypothyroidism. Here are a few references to support this assertion:
Until November 2002, doctors had relied on a normal TSH level ranging from 0.5 to 5.0 to diagnose and treat patients with a thyroid disorder who tested outside the boundaries of that range. Now AACE encourages doctors to consider treatment for patients who test outside the boundaries of a narrower margin based on a target TSH level of 0.3 to 3.0. AACE believes the new range will result in proper diagnosis for millions of Americans who suffer from a mild thyroid disorder, but have gone untreated until now.
Even though a TSH level between 3.0 and 5.0 uU/ml is in the normal range, it should be considered suspect since it may signal a case of evolving thyroid underactivity.
…given the high prevalence of mild (subclinical) hypothyroidism in the general population, it is likely that the current upper limit of the population reference range (for TSH) is skewed by the inclusion of persons with occult thyroid dysfunction….
…In the future, it is likely that the upper limit of the serum TSH euthyroid reference range will be reduced to 2.5 mIU/L because >95% of rigorously screened normal euthyroid volunteers have serum TSH values between 0.4 and 2.5 mIU/L….
A serum TSH result between 0.5 and 2.0 mIU/L is generally considered the therapeutic target for a standard L-T4 replacement dose for primary hypothyroidism.
Demers LM, Spencer CA. NACB. Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. Published guidelines. Online at The National Academy of Clinical Biochemistry (NACB) / The Academy of the American Association for Clinical Chemistry (AACC)
…high thyroid stimulating hormone (TSH) (>2 mU/l) was associated with an increased risk of future hypothyroidism….The simplest explanation is that thyroid disease is so common that many people predisposed to thyroid failure are included in a laboratory’s reference population, which raises the question whether thyroxine replacement is adequate in patients with thyroid stimulating hormone levels above 2 mU/l.
Weetman AP. Hypothyroidism: screening and subclinical disease. Brit Med J 1997;314:1175 (19 April)
Vanderpump MP, Tunbridge WM, French JM, et al. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clin Endocrinol (Oxf) 1995 Jul;43(1):55-68.
For more references that explain why hormone levels “just within the normal range” often aren’t adequate, and why optimizing just T4 (levothyroxine, commonly as Synthroid) without T3 is also not adequate, please see the THYROID STUDIES page.