The Thyroid Sourcebook (5th Edition) - Softcover

Rosenthal, M. Sara

Softcover

ISBN 10: 0071597255 ISBN 13: 9780071597258

Publisher: McGraw Hill, 2008

Synopsis

The classic reference guide for living with thyroid disorder--now completely revised and updated

The New York Times called this book "an excellent source of information." The Thyroid Sourcebook features patient narratives; information on the complications of hypo- and hyperthyroidism, such as depression, weight gain, thyroid, eyedisease, and sleep disorders; the latest on complimentary medicine; and much more.

About this title

About the Author

M. Sara Rosenthal, Ph.D., is a thyroid cancer survivor, bioethicist, medical sociologist, and pioneer in consumer health writing who has authored more than thirty books. She completed her Ph.D. at the University of Toronto and is the director of the Program for Bioethics at the University of Kentucky.

Excerpt. © Reprinted by permission. All rights reserved.

The Thyroid Sourcebook

By M. Sara Rosenthal

The McGraw-Hill Companies, Inc.

Copyright © 2009 M. Sara Rosenthal
All right reserved.
ISBN: 978-0-07-159725-8

Contents

Chapter One

Meet Your Thyroid Gland

A Beautiful Butterfly

An endocrinologist in South Dakota shared a story that illustrates how in the dark most of us are about our thyroid glands. He was treating a new patient for a thyroid condition and explained what the thyroid gland is, how it works, and what it does. The patient was fascinated by this new, critical body part she never realized she had and asked the doctor, "Do cows have thyroid glands? Or other animals?" "Yes," he answered, "all animals, fish, birds, and most other species have thyroid glands." As a newly practicing endocrinologist, he was surprised that this patient was completely unaware of her thyroid gland. But this is not unusual—most people are not aware of their thyroid glands unless they are diagnosed with a thyroid disorder.

Approximately 12 percent of the entire adult population worldwide suffers from some sort of thyroid disease. In the United States, this translates into roughly thirty million adults. Thyroid diseases are grouped by type, such as hypothyroidism, hyperthyroidism, and thyroid cancer. Twenty percent of all women will develop autoimmune thyroid disease, usually hypothyroidism, at some time in their life. Nearly one-fifth of all people over sixty have subclinical hypothyroidism, or mild hypothyroidism.

The purpose of this chapter is to describe where the thyroid gland is located, what it does, and how it works. It also briefly explains the most common thyroid disorders. In addition, it addresses some common misinformation that can interfere with proper decision making regarding your thyroid health. (For information on how to evaluate whether the information you find in various sources is correct, see Appendix A.) The idea is to provide you with enough information about the thyroid gland so you can better understand your diagnosis and make fully informed treatment decisions with your doctor. Since this chapter serves as a very general introduction to the thyroid gland, it will refer you to other chapters in the book for more details.

How Your Thyroid Works

The thyroid gland is often referred to as a butterfly-shaped gland, but it is also shaped like the capital letter H, specifically, the H of the Honda vehicle logo. Each side of the H or butterfly is called a lobe, while the center (the body of the butterfly) is called the isthmus. The thyroid gland is located in the lower part of your neck, in front of your windpipe, and is basically wrapped around the windpipe (see Figure 1.1). Using the butterfly analogy, the butterfly "hugs" the windpipe.

The thyroid gland makes two critical thyroid hormones. The first is thyroxine, known as T4, which has four iodine atoms for each hormone molecule. The second is triiodothyronine, or T3, which has three iodine atoms for each hormone molecule. Both hormones are referred to in the singular as thyroid hormone.

Thyroid hormone is essential for our existence, affecting every single cell in the body. Thyroid hormone serves as the speed control for our cells, controlling their "speed of life." Of the two hormones, it is thought that only T3 has a direct effect on the cells of the body; it is debatable whether T4 has any direct effect. T4 must be converted to T3 by the cells by removing one specific iodine atom before it can work. If a different iodine atom is removed from T4, it creates an inactive molecule that does not work as an effective thyroid hormone. Nearly all cells have special enzymes inside of them called deiodinases that remove the iodine atom from T4 to make it into T3. It is thought that this is one way that each cell customizes how much T3 it will get, even though the blood supply to all the cells generally provides the same level of T4 at the same time. The T3 produced in the body's cells works in the nucleus of these cells to turn some genes on and some genes off. This is how the thyroid hormone works in the body.

For example, in the cells of the pituitary gland (where thyroid-stimulating hormone (TSH) is produced), T3 turns off the gene that makes TSH. This is why TSH levels are high when thyroid hormone levels are low and TSH is decreased when thyroid hormone levels are high.

The thyroid gland usually releases around 80 percent of its thyroid hormone as T4 and 20 percent as T3. Only 0.03 percent of the total T4 traveling around in the bloodstream is in the free form, in which it can be taken up into each body cell and do the job of effective thyroid hormone. Once the free T4 passes into a body cell of any kind, it is changed into T3 by an enzyme called 5-prime deiodinase.

Once changed, this T3 is absorbed into the nucleus of the cell, where the chromosomes are found. Inside the nucleus are special T3-receptor proteins that are made to stick to distinct spots in the genes of the chromosomes and also to stick to T3. When enough T3 is taken into the nucleus, it sticks to these T3-receptors and controls the genes that they are attached to. Some genes are turned on while other genes are turned off. Thus, each cell is able to convert the correct proportion of T4 to T3 for its own needs.

Be Informed: Know the Facts About T4/T3

Many Internet sites and books falsely state that many people cannot convert T4 into T3. Converting T4 into T3 is necessary for life, and there is no evidence that this metabolic derangement can be acquired later in life. Anyone who could not convert T4 into T3 would not be alive, as this conversion is necessary for fetal development and birth.

This myth leads patients into potentially dangerous decisions about their treatment and into purchasing thyroid "support products" or T3 that they may not need. For information on how T3 levels are determined by measuring levels of the thyroid-stimulating hormone (TSH), see page 20.

The T4/T3 conversion myth is also used to support other false statements. One is that TSH tests can read as normal when you're really hypothyroid (this is false except for rare people with pituitary tumors). Another falsity is that dessicated pig thyroid hormone (sold as "natural" thyroid hormone), questionable herbal concoctions that "help" with T4/T3 conversion, or regular and chronic T3 supplementation is preferable to, or healthier than, taking levothyroxine alone at the appropriate dose.

* * *

Be Informed: The Truth About Reverse T3

Many websites and books say that trauma and stress can create a "fake" normal T3 level, called reverse T3. The claim is that many people with so-called normal TSH levels really have reverse T3 and are actually hypothyroid. This theory takes fact and creates fiction.

T4 is converted to T3 by removing a specific iodine atom from each of the T4 molecules. If a different iodine is removed, reverse T3 is formed. Reverse T3 is inactive; it cannot do the job of T3 and therefore will not suppress TSH. It will not affect TSH levels at all. If T4 is converted to reverse T3 without making enough regular T3, your TSH levels will be high and you will be hypothyroid. If the TSH levels are normal, so are the levels of regular T3 inside of your cells.

* * *

The Role of Iodine in the Diet

T4 and T3, as already noted, are so named because of the number of iodine atoms per hormone molecule. So what is the role of iodine in the production of thyroid hormone? The thyroid gland needs to import one key ingredient for thyroid hormone production: iodine. Your thyroid gland extracts iodine from various foods, including fish, egg yolks, shellfish, milk products, and anything with iodized salt. Normally you take in sufficient iodine through your diet.

Thyroid glands are very sensitive to iodine. When the thyroid gland is not able to obtain sufficient quantities of iodine, you can develop a goiter, or an enlarged thyroid gland. A goiter can also develop if your thyroid gland is stimulated to take up too much iodine and produces too much thyroid hormone. Although it seems odd that too much or too little iodine can produce the same results, the reason the goiter develops in each case is different. The role iodine plays in the diet as well as the consequences of iodine deficiency are discussed more in Chapter 11.

The Role of the Pituitary Gland and Thyroid-Stimulating Hormone

The pituitary gland is situated at the base of the skull and is, without question, the most influential gland in your body. It is often referred to as the master gland. The pituitary gland acts as the body's "thermostat" by sending out many types of stimulating hormones to the various parts of our bodies that make hormones.

Your thyroid gland reports directly to the pituitary gland, which monitors T4 and T3 levels in your body. When levels are low, it secretes TSH; this signals the thyroid gland to make thyroid hormone. The TSH stimulates the thyroid to take up iodine from the blood and make thyroid hormone, just as a thermostat's electrical signal to the furnace stimulates it to take up fuel and make heat. When the thyroid hormone level in the blood rises to the proper level, it causes the pituitary to reduce its release of TSH, just as a thermostat turns off its electrical signal to the furnace. This regulates the thyroid hormone in the blood so that it stays at the proper level, in the same way the thermostat keeps a house at the proper temperature.

If the pituitary gland is working properly, a high level of TSH means that there is not enough thyroid hormone in the blood; a low level of TSH means that there is too high a level of thyroid hormone in the blood; and a normal level of thyroid hormone results in a normal level of TSH. The TSH level in the blood can be measured to tell whether the thyroid is making enough, too little, or too much thyroid hormone. The TSH test is the most accurate and sensitive blood test that exists for thyroid patients.

The Role of the Hypothalamus

The hypothalamus is a part of the brain located just above the pituitary gland. It is connected to the pituitary by a thin stalk that carries hormones that help control the pituitary. A part of the hypothalamus also works like a thyroid hormone thermostat, releasing its own signal, thyrotropin-releasing hormone (TRH), or TSH-releasing hormone, to the pituitary when the thyroid hormone levels are low. Thus there is a "double- thermostat" control of thyroid hormone in the body, although this can break down when something is wrong with the hypothalamus.

The Role of Calcitonin

In the thyroid gland, the cells that produce thyroid hormone are called follicular cells. Thyroid follicles are contained within the capsule of the thyroid gland like bunches of microscopic grapes. Between neighboring thyroid follicles are tiny blood vessels, lymph vessels, and collections of other cells, called parafollicular cells. These parafollicular cells, or C-cells, make additional hormones, such as calcitonin and somatostatin.

Calcitonin helps to regulate calcium and therefore helps to prevent osteoporosis. But to your bones, calcitonin is kind of like a tonsil. It serves a useful purpose, but when the hormone is not manufactured due to the absence of a thyroid gland (if it's removed or ablated by radioactive iodine), you won't really notice any effects, just as you don't miss your tonsils. Calcium levels are really controlled by the parathyroid glands and are much more dependent on Vitamin D, which helps with calcium absorption; diet; and exercise, which builds bone mass.

Calcitonin is only important when discussing the thyroid in the context of a rare type of thyroid cancer known as medullary thyroid cancer (see Chapter 6). When this type of thyroid cancer develops, your thyroid overproduces calcitonin, which is a marker for medullary thyroid cancer.

A Few Words About the Parathyroid Glands

There are usually four (though sometimes three to six) other glands located very close to the thyroid gland; they are called parathyroid glands, which literally means "near the thyroid." These glands do not produce thyroid hormone but instead make parathyroid hormone (PTH), which is important for controlling calcium in the body. It causes the kidneys to retain calcium in the blood while releasing phosphorus into the urine. At the same time, it increases the activation of vitamin D, which enhances the absorption of calcium and phosphorus from food and beverages.

These glands are sometimes damaged or accidentally removed during surgery on the thyroid gland. Although only one functioning parathyroid gland is needed, loss or damage to all four glands results in loss of parathyroid hormone, which reduces the absorption of calcium, causing calcium levels in the blood to fall. The symptoms of low calcium include muscle cramps and spasms, numbness, and, in severe cases, seizures. Likewise, losing the parathyroid glands causes phosphorus levels to stay high because the kidneys are not able to release it into the urine.

Damage to the parathyroid glands is a known risk of thyroid surgery. This risk is higher, however, when the surgeon is less experienced, when there is a need for multiple neck surgeries, or when a thyroid cancer is particularly invasive.

The Role of Thyroglobulin

Although this sounds like a Halloween candy, thyroglobulin (Tg) is a specific protein made only by your thyroid cells and is used mostly by the thyroid gland itself to make thyroid hormone. The only role thyroglobulin plays in the treatment of thyroid disease is as a screening marker for thyroid cancer recurrence. After your thyroid gland is removed as a consequence of any type of thyroid cancer (see Chapter 6), the protein thyroglobulin should not be manufactured anymore. If thyroglobulin is detectable on a blood test, it's a sign that some thyroid tissue remains, which could indicate a recurrence of thyroid cancer. Screening for thyroglobulin is useless for all other forms of thyroid disease.

Thyroid Disorders and Treatments: An Overview

The following is a summary of the most common thyroid disorders and their treatments, which will serve as a map to the rest of the book.

Hypothyroidism

Hypothyroidism is an underactive thyroid gland. If your thyroid gland is underactive and manufactures too little hormone, your bodily functions slow down. You'll have an unusually slow pulse, you'll feel very tired, and you'll have no energy. In addition, you might be constipated, you might get a little puffy, you might feel cold all the time, and your skin might get very dry. The most common cause of hypothyroidism is Hashimoto's thyroiditis, an autoimmune thyroid disease. Another common cause is aging; people over age sixty are vulnerable to mild hypothyroidism, which can be easily masked as fatigue associated with aging. See Chapter 2 for more details on hypothyroidism.

Hyperthyroidism

Hyperthyroidism is an overactive thyroid gland. If your thyroid gland is overactive and manufactures too much thyroid hormone, you will become thyrotoxic—toxic from too much thyroid hormone—and your body/heart rate will speed up. You might also feel hot all the time, have diarrhea, lose weight, and feel dizzy or shaky. This is known as thyrotoxicosis, discussed at length in Chapter 3. Hyperthyroidism is a common cause of thyrotoxicosis, but there are other causes as well. The most common is Graves' disease, an autoimmune thyroid disease that causes hyperthyroidism, which then causes thyrotoxicosis.

Another common cause of thyrotoxicosis is taking too much thyroid hormone, taking an unstable formulation of thyroid hormone (as in animal thyroid hormone), or taking T3 supplements (usually unnecessarily). Hyperthyroidism is discussed more in Chapter 3.

Thyroiditis

Thyroiditis is inflammation of the thyroid gland. Depending on what kind of thyroiditis you have, a goiter and symptoms of thyrotoxicosis or hypothyroidism can develop. Hashimoto's thyroiditis is an autoimmune disorder (see Chapter 2). The flulike de Quervain's thyroiditis, silent thyroiditis, and postpartum thyroiditis are usually temporary in nature. Acute suppurative thyroiditis is a bacterial thyroiditis usually seen in children. And Riedel's thyroiditis is caused by scar tissue. These forms of thyroiditis are discussed in Chapter 4.

Goiter

A goiter is an enlarged thyroid gland, and it is a sign that you may be hypothyroid or hyperthyroid. In previous generations, goiters were the way thyroid disorders were usually diagnosed; the appearance of the goiter was the telltale sign. Today, sensitive assay tests such as the TSH can usually diagnose thyroid diseases early, before the goiter appears. Goiters are discussed throughout the book, particularly in Chapters 2, 3, and 11.

Multinodular Goiter

A multinodular goiter is a bumpy or lumpy enlarged thyroid gland. For some unknown reason, one or more nodules, or lumps, form in your thyroid gland. These nodules can be "runaway trains" that mimic the thyroid gland, but they are not controlled by the thermostat system of the pituitary gland or the hypothalamus. The result is thyrotoxicosis. Many times, nodules do not make thyroid hormone. Ten percent of them turn out to be thyroid cancer. Nodules and multinodular goiters are discussed in Chapter 5.

Thyroid Cancer

Thyroid cancer is now the most quickly increasing type of cancer in both sexes and in all ages. There are several types of thyroid cancer, including follicular, papillary, and medullary. Treatments and follow-up care are discussed in Chapter 6.

Complications and Comorbidities

Thyroid disorders can affect other parts of your body. Thyroid eye disease, for example, is a condition marked by bulgy, watery eyes, frequently predates the diagnosis of Graves' disease. Cardiovascular diseases, sleep disorders and fatigue, and depression can all mask, complicate, or accompany thyroid disorders. And thyroid diseases can be aggravated by other factors, such as menopause or age. For the ins and outs of thyroid disease complications and comorbidities, see Chapter 7.

Thyroid Disease and New Life

Creating and bringing a new life into the world can be exciting. However, it can also bring on or complicate thyroid disorders. Infertility can be a result of thyroid disorders, while gestational hyperthyroidism and gestational hypothyroidism can also occur (gestational refers to during pregnancy). Women need to monitor their thyroid levels during pregnancy not only for their own sake, but also for their baby's healthy growth and development. Thyroid disorders in the context of fertility, pregnancy, and in newborns are discussed in Chapter 8.

(Continues...)

Excerpted from The Thyroid Sourcebookby M. Sara Rosenthal Copyright © 2009 by M. Sara Rosenthal. Excerpted by permission of The McGraw-Hill Companies, Inc.. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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Edition details

• Publisher: McGraw Hill
• Publication date: 2008
• Language: English
• ISBN 10: 0071597255
• ISBN 13: 9780071597258
• Binding: Paperback
• Edition number: 5
• Number of pages: 272