What is Grave's Disease? (a layman's explanation)
I should start by stating that I am not a doctor, nor do I pretend to be. I have been living with Grave's for several years, and have done some research on the subject to satisfy my own understandings...
According to the American Association of Autoimmune and Related Diseases (AARDA), it takes an average of 7 years and 5 docs before most autoimmune diseases are properly diagnosed. Hyperthyroidism is not exactly 'common', but it isn't rare either. One report I read mentioned that 1/4 of 1% of Americans have this condition. Also it is about 8:1 female to male, so being a man I guess I'm really unique! We won't go there....
Without trying to get too complicated, the thyroid is a little pear-shaped gland that sits at the base of the throat and wraps around the windpipe. The thyroid produces two hormones known as T3 and T4. About 80% of the hormone produced is T4, and about 20% is T3, but T3 is about four times as 'strong' as T4. The thyroid's hormones control many aspects of the body, including heart rate, metabolism, and a whole pile of other things. The pituitary gland, located at the base of the skull secretes a hormone called TSH (thyroid stimulating hormone) that controls the normal function of the thyroid, telling it how much hormone to produce. The production of TSH is controlled by a part of the brain called the hypothalamus. The hypothalamus produces a hormone called TSH releasing hormone, or TRH. The levels of T3 and T4 are constantly monitored by the pituitary and the hypothalamus and the levels of hormones required are adjusted accordingly in one big loop. Think of the body as a house, and the thyroid gland is the furnace. Someone (the hypothalamus) decides that the house is too cold, so the hypothalamus turns up the thermostat (the pituitary). The thermostat sends a signal to the furnace (the thyroid gland), telling it to put out some heat to the house (the body). When the right temperature is reached in the house (body) the furnace shuts off.
There is also a lymphocyte (another type of cell) called thyroid stimulating antibody that in 'normal' people (never been normal in my life!) is kept in check by other helper and suppresser lymphocytes and killer cells. Actually, I believe there are eight or nine thyroid antibodies. For reasons that I don't think anyone has established, in some people this thyroid stimulating antibody gets out of control in the body, and instructs the thyroid gland to start producing a LOT more hormone than normal. There is a receptor site on the thyroid gland for TSH, and this antibody attaches itself to this site. Because the body is in effect attacking itself, Grave's Disease is called an autoimmune disorder. Blood tests on people with Grave's will show that their T3 and T4 levels are high, and the TSH level is almost non-existent. The pituitary isn't sending any signals to the thyroid, but the antibody is keeping the thyroid working overtime. There are also other reasons for the thyroid to produce too much hormone, including a disease called Hashimoto's disease, or cancer of the thyroid. In some people only a part of the thyroid gland, a nodule becomes overactive.
Symptoms of Grave's disease are many and varied, depending on the person. Most people experience a rapid heart rate and accompanying stress. Most people lose weight, often rapidly, but some people actually gain weight. Tremors, especially in the hands, are common. There are sometimes problems associated with the eyes, specifically pressure on the back of the eyes, causing them to bulge out. Often the thyroid gland will become enlarged and develop into a goiter. Some people develop skin problems, and there are other symptoms as well. Not all of the symptoms are physical, and people with Grave's disease can be affected physiologically as well. This can cause mood swings, short temper, etc., akin to being under a lot of stress. Basically, the whole person is on overdrive, not just the body. Long term problems include a weakened heart muscle, loss of bone density, etc.
Okay, as to what to do about it, allopathic (western) medicine has three basic ways to deal with it. Different people are treated in different ways. Each has its own pros and cons.
The least invasive method is to take a medication that inhibits production of the thyroid hormone. The most common of these is a drug called propylthiouracil but there are others. There is also a class of drugs called beta blockers which will alleviate the rapid heart rate symptoms but don't do anything for the thyroid specifically. Different people have different reactions to these medications. I have a friend who has been taking PTU for a lot of years, and she has dramatically reduced her dosage through time. Some people take the drug to alleviate the symptoms, but when the amounts of the drug are lowered, symptoms recur. Some people have allergic reactions, including skin rashes and outright rejection, and some people just don't respond to the medication at all. There are also some concerns about long term toxicity affecting the liver and other parts of the body from taking this drug for a lot of years.From the Hyperthyroid E-mail List:
"Upon my diagnosis, I started taking PTU and quickly developed liver disease from the drug. While taking PTU, I also discovered that the drug has been categorized by the U.S. Department of Health and Human Services as a "probable carcinogen." You can access that report on the internet by searching for "national toxicity report" or "national toxicity program" or by visiting the U.S. Department of Health and Human Services web site. In lab rats, PTU caused thyroid cancer in rats and another study following people taking PTU discovered that 4 out of 350 (approx., writing from memory)
developed thyroid cancer after long periods of PTU. Keep in mind that estrogen is listed as a probable carcinogen too -- my point is that taking PTU doesn't mean you'll get cancer, but that long term exposure appears to increase your risk for thyroid cancer, much as unusual exposure to estrogen increases risk of ovarian cancer (that's why using fertility drugs like clomid increase one's risk of ovarian cancer).Both PTU and tapazole fall into the same drug family, but aren't exactly the same. For example, PTU is the drug (ironically at least and perhaps dangerously) believed to be safest for pregnant and nursing women and since I was nursing while diagnosed, it was assigned to me. Tapazole can cause an unusual condition in pregnancy, in which the fetus' skin on the scalp doesn't develop and the brain is exposed. However, this is rare -- but possible -- and tapazole is diagnosed during pregnancy outside of the United States."
RAI (radioactive iodine treatment) is probably the most common form of 'treating' hyperactive thyroids. Since the function of the thyroid gland is largely controlled by iodine (BTW, a difference of 3/1000 of an ounce of iodine in the body can spell the difference between health and disease), a dosage of radioactive iodine is administered - usually through a liquid or a pill form. The radioactive iodine targets the thyroid gland, and will often kill the entire thyroid gland over time. People who undergo the RAI treatment will usually have to take synthetic thyroid supplements for the rest of their life. The amount of iodine given will vary depending on body mass and a number of factors. People who have undergone RAI will have to maintain a distance from others, especially children, for a few days, use separate glasses, plates, utensils, etc. and flush the toilet 3 or 4 times after use in that initial period as the radioactive iodine is flushed from their body. It is important to remember iodine isn't exclusively absorbed by the thyroid gland; although the thyroid gland absorbs most iodine; other sites are skeletal muscle, skin, pancreas, salivary glands, stomach mucosa, breast tissue. Some people with hyperthyroidism have difficulty tolerating iodine; some people even get boils, as well as flushing and increased iodine absorption to cell receptors in the skin. Undergoing RAI treatment targets ALL of these regions and more.
Some people have had to undergo 2 or 3 RAI treatments to complete the job of killing off the thyroid gland. There is also a greater risk of thyroid related opthalmic problems (known as thyroid eye disease, or TED) after RAI. Some studies indicate that RAI can cause increases in cancers and other disease, and genetic disorders that may not be revealed for years. Side-effects in some people include itchy scalp, hair loss, nausea, excessive weight gain, bloating, joint pains, initial wide swings in hormone level, some people go from being hyper to hypo and back to hyper, etc. until their required level of medication is sorted out. In some people these symptoms can last 6 months or more. After becoming hypothyroid, there are associated problems as well.Thyroid surgery is the most invasive form of 'treatment', and is usually reserved for the more extreme cases. All or part of the thyroid gland is removed during surgery, and most people become hypothyrodic and have to take synthetic thyroid supplements for the rest of their life to balance this. There have been a lot of advances in surgical techniques in recent years, but there is still a small risk of a person losing all or part of their voice. In some cases people retain their speech, but their vocal tone becomes lower.
Because of the associated eye problems, in some cases people have to go through radiation treatments, radial compression surgery or other ophthalmic surgery to correct the 'bulging eyes' condition.
I've been doing some lay research recently (no you don't lay around and research things) on the link between Grave's disease and osteoporosis, and I think I've found something. I'll try not to make it too complicated...
At first glance, the thyroid gland has nothing to do with calcium, bones, or osteoporosis. The thyroid gland produces hormones that affect heart rate, metabolism, etc. - the 'fire' of the body's furnace. Calcium levels in the body are strictly controlled by something else, called the parathyroid. There are four parathyroid nodules, located behind the thyroid gland at the base of the neck. Although they are anatomically very close, the two don't have any obvious relationships with each other.
The parathyroid monitors and controls calcium levels in the body. That's its job, and that's all it does. About 99.5% of the body's calcium is held in the bones, and the rest floats around the bloodstream and other places. Having an imbalance of calcium can have a lot of effects - too little and the body takes calcium from the bones to compensate - too much, and it can have effects on the stomach lining, pancreas, kidneys, etc. Because the kidneys filter blood of impurities, having too much calcium in the blood can lead to deposits and kidney stones. In rare cases one can develop calcium deposits on the back of the heart and other places.
The parathyroid works with other aspects of the body in an intricate relationship. Levels of parathyroid hormone determine how well the wall of the intestines absorb calcium from what you eat, how much calcium is excreted from the kidneys through your urine, and how much calcium is given to or taken from your bones.
Bones are living tissue, and there are two different types of cells involved in bone growth. Osteoclasts chew up old bone, and osteoblasts make new bone. As people age, the rate of the osteoclasts starts to outpace the osteoblasts, so that the body loses slightly more bone than it makes. A number of factors can contribute to this. Having an overactive parathyroid gland is one of them - if the parathyroid is producing too much hormone, the osteoclasts work overtime.
So what does this have to do with the thyroid gland and Grave's disease? As far as I can tell, nothing. However, aside from T3 and T4, the thyroid gland produces a hormone called calcitonin. Calcitonin in the body has some effect on slowing the action of the osteoclasts and results in less bone loss. Can't say for sure, and others are welcome to join in here, but if having an overactive thyroid gland lowers the levels of calcitonin, that may be a link.
Someone else with Grave's sent me the following:I have been wondering what happened to the calcitonin production in my body when the thyroid was zapped with RAI.
Research indicated that the part of the thyroid that makes calcitonin is very sensitive to radioactivity and is likely to have been destroyed (although sometimes some remains and recuperates). This raises the question of what happens to me when I don't have this source of calcitonin (CT). My (former) endocrinologist said that CT neither causes nor cures any disease. This drove me to further research. It seems that CT, in slightly different forms, is made in other parts of our bodies because it is vital. However, my internist tested my CT levels and they are low. I don't know the implications of this. CT was out of style in medical research for a while, but it seems to be coming back. It is, after all, used to treat osteoporosis.
The other thing I worried about is the effect of RAI on the parathyroid glands, since they are basically imbedded in the thyroid. Research showed that they are in fact affected by radioactivity, although it usually takes time (years?) for the effects to show up. The response is for one or more of the parathyroid glands (PT) to become enlarged (an adenoma or hyperplasia) and put out too much hormone. The hormone triggers too much calcium in the blood. This can cause a lot of bad effects on our bodies.
In addition, there is a correlation between hypothyroidism and hyperparathyroidism (too much PT hormone). There may also be a link between ATDs and hyperparathyroidism (a few studies). Symptoms of hyperparathyroidism include bone and muscle pain, depression, brain fog, digestive problems, and more (not hair loss, I don't think). A lot of them are like hypothyroid symptoms.
We should all have our intact calcium blood levels checked periodically. We should all have our parathyroid hormone levels checked, too, although that test is expensive and has to be sent to a specialized lab. My calcium levels have been bouncing around the normal range, but my parathyroid levels are quite high. There is debate (between me and the doctors) about the implications of this.
From Endocrine Diseases: thyroid, parathyroid, adrenal and diabetes I found the following:"Remodeling consists of tearing down small parts of the bones, and then re-forming them. The breaking down portion is termed "resorption" and is performed by large cells within the bones called "osteoclasts". Osteoclasts live in the central portion of the bone. They are continually removing small (microscopic) portions of bone at the edge of the bone surface. Nearby, bone forming cells called "osteoblasts" begin to fill in the holes left behind. Here is the big problem: remodeling does not seem to be a perfect give and take of bone mass. The osteoblasts are less efficient at making bone than the osteoclasts are at removing it. Although the difference is slight, this is what accounts for the gradual loss of bone density (BMD) as a person ages. Any factor which causes a higher rate of bone remodeling will ultimately lead to a more rapid loss of bone mass and thus more fragile bones....
....Calcitonin is a hormone which is naturally produced in the thyroid. Calcitonin is a powerful inhibitor of osteoclastic activity (the cells which continuously reabsorb bone). When given to patients with osteoporosis, calcitonin produces modest increases in bone mass.
On the other hand, some doctors feel that there is no connection between calctonin and bone loss.
From BASIC AND CLINICAL ENDOCRINOLOGY by Greenspan and Strewler, copyright 1997: p. 271: "Although its secretory control by calcium and its antiresorptive actions enable calcitonin to counter PTH in the control of calcium homeostasis, thus engendering bihormonal regulation, it is actually unlikely that calcitonin plays an essential physiologic role in humans and other terrestrial animals. This surprising conclusion is supported by two lines of evidence. First, removal of the thyroid gland -- the only known source of calcitonin in mammals -- has no perceptible impact on calcium handling or bone metabolism. Second, secretion of extremely high calcitonin levels by medullary thyroid carcinoma, a malignancy of the C cell, likewise has no apparent effect on mineral homeostasis. Thus, in humans, calcitonin is a hormone in search of a function. It plays a much more obvious homeostatic role in salt-water fish, in which the major challenge is maintenance of blood calcium levels in the sea, where the ambient calcium concentration is very high. Calcitonin is of clinical interest for two reasons. First, calcitonin is important as a tumor marker in medullary thyroid carcinoma....Second, calcitonin has found several therapeutic uses as an inhibitor of osteoclastic bone resorption."
From TEXTBOOK OF ENDOCRINE PHYSIOLOGY, edited by Griffen and Ojeda, copyright 1996, p. 327: " The physiological significance of calcitonin in humans has been questioned because there is no known metabolic consequences of calcitonin deficiency or excess. Serum calcium is well regulated within normal limits after total thyroidectomy..."
A complicated question, with no easy answers.
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