Authors: Rita Baron-Faust,Jill Buyon
I really had no idea anything was wrong with my thyroid until I literally passed out in the street and had to be taken to the emergency room. The doctors said it was a “thyroid storm.” The way they explained it, it was like driving a car with the gas pedal pushed all the way down to the floor. My body was speeding along and just crashed. I had always been a “hyper” person, always active, always fidgety. I had a high pulse rate, I was skinny. But up until I collapsed, I didn’t think anything of it. That’s just the way I was.
A
NNE
M
ARIE
, 36
T
he thyroid is a butterfly-shaped gland located in the neck, just below your voice box. Although it’s small—a little more than two inches wide—the thyroid gland plays a big role in the body. Thyroid hormones influence almost every organ and regulate metabolism, the rate at which the body converts food into energy.
Having thyroid disease is akin to living in a house where the thermostat doesn’t work properly—it’s either set too high, turning up the heat and making you feel jumpy, or set too low, making you feel cold and tired.
The thyroid is part of the
endocrine system
, a network of glands that secretes hormones right into the blood, rather than piping them in through a network of ducts. The other endocrine glands are the pancreas, the pituitary, the adrenals, the parathyroids, and the ovaries—all of which can be the targets of autoimmune attacks.
The pituitary gland (located in the brain just behind the eyes) is known as the “master gland” because it regulates the other endocrine glands, including the thyroid. The master gland has a master switch, and that’s the hypothalamus, a tiny area in the base of the brain connected to the pituitary. Secretion of just the right amount of thyroid hormones is governed by a feedback system between these three structures.
The hypothalamus sends out a hormone called
thyrotropin releasing hormone (TRH)
, which prompts the pituitary to release
thyroid stimulating hormone (TSH)
, triggering the secretion of thyroid hormones by the thyroid gland. There are two thyroid hormones:
thyroxine (T4)
and
triiodothyronine (T3)
. Thyroxine is produced by the follicular cells of the thyroid and converted to T3 by enzymes in various organs (some T3 is produced by the thyroid, too). If thyroid hormones in the bloodstream rise above normal levels, they cause a decrease in TRH and TSH that prompts the thyroid to cut back on the amount of hormones it secretes. If thyroid hormone levels drop below normal, the hypothalamus increases secretion of TRH, which prompts the pituitary to pump out TSH to stimulate the thyroid.
This feedback loop is like a thermostat, constantly keeping thyroid hormones at just the right level (this is called
euthyroid
). When the immune system attacks the thyroid, it leads to overproduction or underproduction of thyroid hormones. Either the heat’s too high, as excess thyroid hormone speeds up energy use and causes weight loss, hyperactivity, sweating, and nervousness; or the heat’s too low, as too little thyroid hormone slows energy use, causing weight gain, fatigue, coldness, and depression.
Thyroid diseases are the most common of all autoimmune diseases, affecting more than 10 million people.
Hashimoto’s thyroiditis
, an
under
active thyroid gland, affects 8 to 10 times more women than men.
1
Graves’ disease
, in which the thyroid becomes
over
active, is five times more common in women.
2
Both can lead to infertility and miscarriage, emerge during or after pregnancy and present a threat to an unborn child, and, in older age, be mistaken for signs of aging. Untreated hyperthyroidism can also lead to bone loss, since excess T3 activates bone-eating cells called
osteoclasts
.
3
In Hashimoto’s thyroiditis, T cells attack the follicular cells in the thyroid gland, causing inflammation that hampers production of thyroid hormones. Healthy thyroid cells are replaced by lymphocytes and macrophages and, eventually, by scar tissue, so little or no hormones are secreted.
4
Autoantibodies (sometimes called
thyroid autoantibodies
) are directed against the contents of the thyroid cells, either thyroglobulin (TG) or thyroperoxidase (TPO), two proteins needed for the production of thyroid hormones. “Whether these antibodies cause the disease, worsen it, or are simply results of thyroid disease has not been fully established,” remarks Noel Rose, MD, PhD, whose initial investigations into the autoimmune basis of thyroid disease in 1956 launched the field of autoimmunity. “Many people have these antibodies with no evidence of clinical disease. So there must be additional factors triggering thyroiditis.”
In Graves’ disease, antibodies attack receptors for thyroid stimulating hormone on the surface of thyroid follicular cells, triggering overproduction of thyroid hormones.
4
These autoantibodies,
thyrotropin receptor antibodies (TPO)
(also called
thyroid stimulating immunoglobulins
or
thyroid stimulating antibodies
), affect every cell in the thyroid, causing the gland to enlarge as it becomes hyperactive. So Graves’ is also called
diffuse toxic goiter
. Antibodies to
thyroglobulin
and
thyroperoxidase
are also found in Graves’ disease.
Graves’ and Hashimoto’s are closely related; women with thyroiditis may eventually develop Graves’ and vice versa. “There’s a phenomenon we call Hashitoxicosis, where patients with Hashimoto’s disease become hyperthyroid because they have the thyroid stimulating antibody as well as the typical thyroid inflammation. And you also have a phenomenon where patients start out hyperthyroid and become hypothyroid,” says Dr. Rose, now at the department
of pathology at Boston’s Brigham and Women’s Hospital and a professor at Harvard Medical School. There may be separate autoimmune processes taking place in the thyroid, but one may be clinically dominant over the other, and this may shift over time.”
Autoimmune thyroid diseases tend to run in families. It’s not uncommon for one family member to have Hashimoto’s and another to have Graves’ disease. A woman with autoimmune thyroid disease in close relatives may have a five- to tenfold risk of developing thyroid disease. Thyroid diseases frequently occur with other autoimmune diseases (see
page 117
).
It’s still not known just what sets off the process that destroys or overstimulates the thyroid. One possibility is that excess iodine in the diet triggers the autoimmune response. Another theory is that fetal cells that enter a woman’s circulation during pregnancy (microchimerism) may play a role in thyroid disease (see
page 13
). Other factors, such as severe stress or smoking in Graves’ disease could be involved.
In some cases, a woman may develop Graves’ disease or Hashimoto’s during pregnancy or after giving birth (see
pages 120
to
121
). One report by the American Thyroid Association (ATA) calls pregnancy “a stress test for the thyroid,” noting that changes in the gland during this period (and accompanying fluctuations in thyroid hormones) can result in hypothyroidism in women with limited thyroid reserves or who are iodine deficient, and postpartum thyroiditis in women with underlying Hashimoto’s who were euthyroid before conceiving.
5
It’s thought that the immune system rebound after pregnancy causes production of autoantibodies (or increases levels of previously undetected antibodies), leading to dysfunction of the thyroid.
When your thyroid produces too little thyroid hormone, it not only slows metabolism but also decreases production of body heat. The body tries to conserve heat by diverting blood flow from the skin, which keeps the skin cool and reduces sweating, preventing the loss of body heat. So women with an underactive thyroid often feel cold (even though their body temperature is normal) and look somewhat pale. Skin may become dry, nails and hair may become brittle, and there may even be hair loss on the scalp and elsewhere on
the body (including the eyebrows, eyelashes, and pubic hair). Hair loss may be so gradual that you don’t even notice it at first.
As the body slows down conversion of food to energy, you may gain weight and feel tired and drowsy. Some of the weight gain comes from fluid accumulation. Muscle contractions in the intestines, which move digested food along for absorption and waste excretion, also slow down, so you may experience hard stools and constipation. An underactive thyroid also leads to elevated cholesterol.
A key symptom of Hashimoto’s is depression, and if you have a persistent low mood you should be tested for low thyroid hormones. Depression is also common in women with multiple sclerosis and lupus, as is difficulty concentrating. Clinical depression is a separate illness and does not accompany thyroid disease. However, women being treated with the mood stabilizer lithium for a form of depression called bipolar disorder (manic depression) may develop hypothyroidism.
Nerve problems can also occur in Hashimoto’s. You may feel tingling or a pins-and-needles sensation in your hands and feet (which may also occur in MS and other neurological disorders).
Carpal tunnel syndrome can also occur, because of tissue swelling and pressure on the median nerve, which passes through a tunnel-like space in the wrist. Carpal tunnel syndrome causes tingling in the hands and fingers, especially at night. The problem is often blamed on repetitive stress, especially if you work at a computer, but it may in fact be caused by an underactive thyroid. You may also have shortness of breath because of a lowered heart rate, muscle aches or cramps caused by decreased blood flow to the muscles, and slow reflexes. These symptoms may be attributed to a coexisting autoimmune disease.
As Hashimoto’s becomes progressively worse, the thyroid can become enlarged, causing a feeling of pressure around the throat when swallowing, so your voice can become hoarse. Menstrual flow can increase and periods may become longer. There may be bleeding between periods and a failure to ovulate, leading to infertility. Women with undiagnosed hypothyroidism are also at risk for miscarriage, premature delivery, stillbirths, and certain birth defects (see
pages 118
to
119
).
All of these symptoms can come on very gradually. “The reserve of the thyroid is huge. So before you may actually present with symptoms of
hypothyroidism, a large proportion of the gland would need to be destroyed,” remarks Dr. Rose.
Anne Marie’s story continues:
After I collapsed, they tested me for everything under the sun. And it was then that I noticed how much weight I was losing and how much I was eating. I was eating everything and dropping weight so quickly. A pound or so every few days. I weigh 120 now, but eight years ago I maybe weighed 99, 100 pounds. I would feel like I was jumping out of my skin. When I had a “1thyroid storm” I felt a kind of madness, and my pulse was pounding. And I had this stare. My eyes were protruding and I was very self-conscious about it. Now I realize I must have had thyroid symptoms for a long time; they must have started very gradually. After I was told my thyroid was overactive, it all made sense to me. But truthfully, I didn’t pay much attention until I had a problem.
While Hashimoto’s causes a slowing down of body functions, Graves’ disease speeds things up. Metabolism increases, causing weight loss. Because the body needs more blood to compensate for increased energy use, the heart must pump faster. So you can have a rapid pulse, palpitations (heightened awareness of a pounding heartbeat in the neck or chest, or a brief episode of rapid heartbeat, even at rest, or a sensation of a skipped heartbeat), sometimes accompanied by shortness of breath.
Excess thyroid hormone can lead to the development of an irregular heartbeat (arrhythmia), including
atrial fibrillation (AF)
, a rapid fluttering of the upper chambers of the heart. AF, which occurs in up to 15 percent of women with an overactive thyroid, can increase the risk of stroke.
6
Because the atria are not pumping properly, blood may stagnate, forming clots that can break off and block blood flow to the brain.
The thyroid “storm” experienced by Anne Marie is very rare—the incidence is thought to be two in one million—but it can be fatal in 11 percent of cases.
As the body produces more heat, sweating increases. If you have an overactive thyroid you may feel warm and flushed and uncomfortable in hot weather
or warm environments. The gastrointestinal system speeds up passage of food through the intestines, so bowel movements become more frequent. As metabolism increases, you feel more energetic, even hyperactive, jumpy, or “wired.” It can become hard to sit still and concentrate, and you jump from task to task (some women describe this as feeling like their “motor is always running”). You may even talk rapidly. The motor doesn’t slow down properly at night, so it may be hard to fall asleep and stay asleep; your mind may still feel like it’s racing. Since you don’t sleep properly, you can become fatigued.
Muscle weakness is also common, especially in the muscles of the hips, thighs, and shoulders. It can be so bad you may have difficulty raising your arms to brush your hair, climbing stairs, or even getting out of a chair. Changes in the skin and nails also occur. Your nails may grow faster, causing them to get soft and tear easily. Skin feels thin and almost silky, and there may be areas of increased (or decreased) pigmentation. In rare cases, women may develop reddish, lumpy, and thickened skin in front of the shins, just above the ankles (
pretibial myxedema
).
2
Hair becomes softer and finer and may begin to fall out. Hair loss may be related to another autoimmune disease, alopecia areata, which causes roundish bald spots on the scalp (
pages 160
to
166
). But more often, it’s thinning hair, which can be extensive. Treatment with thyroid hormone usually stops hair loss.
The emotional symptoms of Graves’ include irritability and wide mood swings. Small annoyances may set off a major reaction. Or you may act manic, with bursts of energy and intense activity. Since this can also be a sign of bipolar disorder, if no other symptoms of hyperthyroidism are present, an evaluation by a mental health professional may be needed.
The thyroid gland often becomes enlarged in Graves’ disease, but may not cause discomfort. In severe cases, where the thyroid grows three to four times its normal size, you may have a feeling of pressure in the neck when swallowing or turning your head.
Menstrual flow may become lighter if you have Graves’ disease, and periods may become shorter; some women may stop having periods altogether (
page 118
).
The hallmark symptom of Graves’ disease is eye inflammation and the development of protruding eyes (
Graves’ ophthalmopathy
). This occurs in about 50 percent of women with Graves’ as the eyes are pushed forward because of swelling and inflammation of muscles around the eye and tissues
behind the eyeballs. It can cause major vision loss if it damages the optic nerve. Increased pressure behind the eye hampers normal blood and fluid drainage, causing swelling of the tissues around the eye and aching or pressure. The eyes may also be red and inflamed. Weakened eye muscles can hamper movement of the eyes, leading to double vision or impaired vision. Eyelids may not close completely at night over protruding eyeballs, causing the cornea to become dry and prone to ulcerations. The severity of these problems usually has nothing to do with the degree of hyperthyroidism and may even occur without significant elevation of thyroid hormones.
2
Symptoms may gradually get better over 6 to 12 months, but there’s no way to predict whether eye problems will improve. Inflammation is usually not permanent, and less than 1 percent of women have serious or permanent problems. Most often, problems are mild, requiring artificial tears to prevent dryness; more severe cases may necessitate steroid medications, radiation therapy, or surgery (see
pages 114
to
115
).