According to the American Thyroid Association, millions of Americans (especially women) suffer from a thyroid disorder, and many of them dont even know it. In fact, thyroid disorders occur much more often than even many doctors realize. The butterfly-shaped thyroid is in the neck, its two wings wrapped around the windpipe just below the Adams apple. This vitally important gland normally weighs less than an ounce, but it can have an enormous impact on your health. Think of it as your bodys metabolism regulator. It does the job by releasing two hormones, most of which is the iodine-containing hormone thyroxine. The hormones help regulate your heartbeat, body temperature, the smooth working of your muscles, how quickly you burn calories, how swiftly food moves through your digestive tract and more.
Normally, the thyroid doles out just the right amount of hormone to keep these processes humming smoothly. But in some cases it may become overactive and pump out too much hormone called hyperthyroidism. And on the other hand it may slow down and produce too little hormone called hypothyroidism.
Most thyroid problems-involving overactive or underactive glands-are caused by an autoimmune reaction. Normally the immune system functions to defend the body from invading microbes. In an autoimmune reaction, however, the immune system turns against the body itself and goes on the attack. In graves disease the antibodies attach to the thyroid receptors and stimulate the thyroid to produce excessive amounts of thyroid hormones. In both cases serious imbalances in the bodys energy regulation system occur. The good news is that both kinds of thyroid problems respond well to treatment after they are diagnosed.
Normally the thyroid gland is located in the front of the neck just below the Adams apple (Bayliss, 1982). This butterfly-shaped gland located at the base of your neck plays a role in your bodys metabolism. By releasing thyroid hormones, the thyroid actually regulates how your body uses fuel (Morgan 1996). The thyroid is an endocrine gland. Other endocrine glands include the pituitary gland, pancreas, ovaries in women and testes in men, the adrenal glands, and the parathyroid glands. The thyroid manufactures certain chemical substances (hormones) that are secreted into the bloodstream and induce an effect on cells and tissues elsewhere in the body (Bayliss 1982).
The thyroid makes two hormones- thyroxine, which because this chemical compound contains four iodine atoms is often called T4, and triiodothyronine which contains three iodine atoms thus calledT3 (Korte 1994). Both are secreted into the bloodstream and carried throughout the body. In many respects these thyroid hormones can be likened in their action to the speed control on a record player. They regulate the metabolic activity of all body cells and tissues. Too little thyroid hormone means that the body cells work at too slow a rate. The result is much the same as playing a 45r.p.m. record at 331/3 r.p.m.; it is slowed and sluggish. By contrast too much hormone induces the cells to work too fast, like playing a 45 r.p.m. record at 63 r.p.m. and the result is the chipmunk effect (Epps 1995). Although the two thyroid hormones influence the proper working of all body cells, their effect is particularly evident in certain functions (Foley 1993). For example growth and development, both physical and mental, depend upon the presence of an adequate amount of thyroxine. Without thyroxine a tadpole will not metamorphose into a frog, and without thyroxine a newborn baby will not grow properly nor will its brain develop properly. Thyroxine regulates the rate of oxygen consumption, which is another way of saying it controls the speed of activity of body cells(Morgan 1996).
The secretory activity of the thyroid gland is regulated by the pituitary glands secretion of thyroid-stimulating hormone (TSH or thyrotrophin). The pituitary gland is the size of a grape and lies at the base of the brain. It secretes many different hormones including the TSH. This hormone passes into the bloodstream and activates the thyroid gland to secrete more T4 and T3 (Thibodeau1992). As a result of this stimulation of the thyroid cells, the level of T4 and T3 in the bloodstream rises; the pituitary cells that secrete TSH sense this and the output of thyroid-stimulating hormone is reduced (Morgan 1996). This feedback control is similar to a thermostat that senses when the temperature in a house has risen to the required degree then turns off the furnace so the heat production is stopped or reduced. Vise versa, when the blood levels of T4 and T3 fall below a certain point, the TSH-secreting cells of the pituitary gland recognize this, and produce more TSH. This activates the thyroid cells to increase their output of T4 and T3 just as when rooms temperature falls below a certain point the thermostat activates the furnace to produce more heat (Bayliss 1992).
Some diseases are specific or particular to the thyroid gland and do not, indeed cannot, occur elsewhere in the body. For example overactivity of the gland and underactivity are, in the symptoms produced, diseases only associated to the thyroid (Thibodeau 1992). Certain other disorders such as acute or subacute inflammation (thyroiditis) and cancers are not so specific to the thyroid because inflammation or malignant change occurs in other organs (Epps 1995).
Hyperthyroidism, also known as thyrotoxicosis, is a clinical state in which increased amounts of the two thyroid hormones thyrocine (T4) and triiodothyronine (T3) are usually present in the bloodstream. Sometimes only the T3 level is raised so called T3 toxicosis.
Causes of Hyperthyroidism (Graves disease) (Bayliss 1992).
The causes of hyperthyroidism are many but in practice 99% of cases are caused by increased secretion of hormones from a gland that is being overstimulated by thyroid-stimulating antibodies (Graves disease or diffuse toxic goiter) (Korte 1994).
The commonest cause of hyperthyroidism is Graves disease. Because all the thyroid cells are made overactive by stimulating antibodies circulating in the bloodstream, the whole gland is hyperactive, and this is shown by a radioactive isotope scan in which the isotope is found uniformly distributed throughout both lobes (Epps 1995). The gland is usually symmetrically enlarged to a moderate degree although it may range from being normal in size to visually obvious enlargement. Certain changes often occur in the eyes of a patient with this primary hyperthyroidism (Graves disease) (Foley 1993).
Thyrotoxicosis due to Graves disease occurs ten times more in woman than in men and the reason for this is unknown. It tends to run in families and those with a particular constitutional body cell type (HLA B8-DRW3) seem most vulnerable. What triggers off the disease is unknown. In some instances Graves disease seems to follow an emotional upset but it has not proved possible to establish scientific proof of such a cause and effect relationship (Morgan 1996).
Tiredness is usually the first symptom of Graves disease, to be followed by weight loss, palpitations of the heart or consciousness of the hearts action, nervousness, apprehension or irritability and increased sweating (Foley1993). The patient feels hot all the time and is uncomfortable in warm weather. There is often generalized itching of the skin. The eye complications are the first and most obvious manifestation of Graves disease (Bayliss 1996).
Progressively patients with Graves disease proceed on to a classified case of hyperthyroidism. Patients with hyperthyroidism are usually thin or show evidence of weight loss. They are restless and anxious. It is hard for them to sit still and they fidget. Their hands are hot and when held outstretched there is a fine tremor-not a course shaking. Because it is overactive and producing too much thyroid hormone, the blood flow through the gland is increased (Thibodeau 1992). This is detected as a swishing murmur when a stethoscope is held over the front of the neck. Often the patient has starey eyes and this may be the first sign that alerts the doctor to the diagnosis (Bayliss 1982).
Involvement and changes of the eyes are common in hyperthyroidism. There is a tendency for the upper eyelids to be pulled upwards, and when the patient looks down the upperlids are slow to follow the eyeballs. Thus the eyes develop a staring quality and they may tend to bulge outwards (Korte 1994). This appearance is due to changes in the nervous control of the upper eyelid and usually disappears as the hyperthyroidism is controlled (Epps 1995). These changes may occur in hyperthyroidism due to any cause, and is not specific to Graves disease (Foley 1993).
There are three main methods in treating hyperthyroidism. These are (1) antithyroid drugs which suppress the ability of the thyroid gland to make T4 and T3, (2) surgical removal of most of the thyroid gland and (3) radio-iodine treatments which is concentrated in the cells of the thyroid gland and by irradiation destroys them (Bayliss 1982).
Which of these three methods is used depends upon a considerable amount of factors that have to be considered in each individual case (Thibodeau 1992). When given antithyroid drugs, constant monitoring by a doctor is necessary. Surgery, though once a common treatment, is really inappropriate in this day and age. So if it is the only option offered, that should be a red flag. The only scenario where surgery may be the only option is if there is an allergic reaction to thyroid drugs. During radioactive iodine treatment capsules containing radioactive iodine destroy part of the thyroid gland (Epps 1992). The treatment always works, is safe and usually requires only a one-time treatment. The radioactive treatment has been used for over 50 years and its safety has been shown over and over again (Thibodeau 1992).
Hypothyroidism is the clinical condition that develops when there is inadequate secretion of thyroxine (T4) and triiodothyronine (T3) by the thyroid gland (Morgan 1996). Irrespective of the cause of the thyroid deficiency, the symptoms and clinical picture in the adult are the same although these vary in their severity according to the degree of the deficiency and its duration. Myxoedema is the word used to describe advanced hypothyroidism (Korte 1994).
There are many causes of deficient thyroid secretion. Two obvious ones are the removal of too much thyroid tissue during the treatment of hyperthyroidism and destruction of too much of the gland in radioactive iodine treatment (Bayliss 1982).
In the Western world Hashimotos thyroiditis is the commonest cause of spontaneous hypothyroidism and is the presumed cause of thyroid failure in patients (Thibodeau 1992). Hashimotos thyroiditis was one of the first autoimmune diseases in medicine to be recognized, and its understanding has thrown light on other autoimmune disorders (Epps 1995). We still do not know why certain white corpuscles come to regard thyroid tissue as foreign, but these lymphocytes with their associated thyroid antibodies attack the thyroid gland and gradually destroy it (Korte 1994).
In some parts of the world iodine deficiency is the most common cause of thyroid failure. Lack of iodine prevents the thyroid from having enough raw materials to manufacture T4 and T3. This condition is usually associated with a sizeable goiter, whereas in the conditions mentioned earlier little or not thyroid tissue can usually be felt (Bayliss 1982).
The severity of the symptoms in hypothyroidism depends upon the degree of thyroid failure and upon its rate of onset. Legarthy is the first manifestation. Intolerance of cold is another early feature. Menstruation in women may be heavier and more prolonged. Some gain in weight is common but usually not more than 10 pounds in one year. The skin becomes dry and the scalp hair may be lost at an increased rate (Korte 1994). The voice becomes deeper in pitch. Hearing is dulled, constipation is common, muscle aches and pains occur, and the patient may become unsteady on his/her feet. The patient may slur words and seem to be in a drunken state. These are all consequence of the slowing metabolism of all cells throughout the entire body (Bayliss 1982).
The best treatment for hypothyroidism is replacement therapy with thyroxine. Though man-made, medicinal thyroxine is chemically identical to the major hormone secreted by the thyroid gland (Baykiss 1982). While there are natural forms of the hormone, most doctors advocate using a synthetic form (i.e. Synthroid). Being a pure substance the amount in each tablet can be accurately measured (Korte 1994). The ultimate final dose of the thyroxine will depend upon the degree of thyroid failure, and to a lesser extent on the weight and responsiveness of the patient (Foley 1993).
Thyroxine does not work fast. A tablet taken, for example, on a Monday will induce no biologically discernible effect until the Following Friday. The tablet is taken everyday, and preferably at the same time each day. Since the thyroid fluctuates the dosage has to be adjusted to the patients symptoms (Morgan 1996). A number of patients give themselves an excessive amount of thyroxine. They increase the dose themselves in the false hope to lose weight or to increase energy. Some patients become addicted and take an amount of thyroxine that makes them hyperthyroid (Epps 1995).
Women get thyroid disease (leading to hyper-or hypothyroidism) ten times more often than men do. Though doctors say there is not much that you can do to prevent thyroid disease, I think its important to recognize it and get it treated in its early stages.
I believe you should first know the symptoms. All of the research on thyroid disease has given us solid clues as to what to be aware of when detecting this disorder. We know that women are more susceptible. A rapid heart rate, increased nervousness or changes in the menstrual cycle and weight loss are indicators of hyperthyroid. On the other hand, sluggishness, weight gain, fatigue and increased intolerance to cold could all point to hypothyroidism.
One big advantage that the research of my topic has produced is the fact that thyroid disease can be inherited. If there is a family history we are now well aware that the chances are increased. Still, to this day I strongly believe that more steps need to be taken in finding a better way to manage thyroid disorders. My mother is afflicted with this disease and the stresses and pain it has brought into our family are immeasurable. The reason I feel so passionately about this issue is that the solutions to this problem have only been temporary. When the thyroid flips in to high gear the dosage of medication needs to be lowered and vise versa. Yet we only know when to change the dosage when she is extremely high or low, and with this comes mental anguish. Depression and other disorders run rampant within the mind of a thyroid patient and it is quite sad.
In all of the materials I researched I found no solid clues to the planned future endeavors by any researchers or scientists in this field. The fact is that with the treatments found most patients are able to live normal lives. The advances and discoveries of synthetic drugs have virtually iliminated the problem. Yet, in my mothers case and a good population more, I feel there is need for a more reliable, versatile treatment that can be prescribed with many other drugs if needed.
If I had the power to establish the next step in thyroid research, I would manipulate the gene. In this day and age we have technology that can isolate and illuminate genes. Researchers know now that there is a predisposed body cell type HLA B8 DRW3, that is most vulnerable to thyroid disorders. I would find the hereditary gene cell type that carries this disorder and manipulate it so we could rule out that possibility.
The next step would be to create a drug similar to Thyroxine and Triiodothyronin and to instill the qualities of fluctuation in them. Instead of the patient going in to the doctors office to get the prescription dosage increased or decreased, (usually after some sort of adverse effects) the pill would have the capability of doing so itself. If this quality is incapable of being present in a pill then the creation of an implant could be applied. The implant along with a microchip would sense and detect the slightest changes in the naturally made T4 and T3 and then it would make up the difference. Ultimately the problem of going hyper and hypo will be eliminated.