Graves Disease Natural Remedies

As a graves disease sufferer, I would say no. You can help your body by reducing the amount of iodine in your foods, but there isn't anything natural that I know of to stop the disease.

The 3 main problems with prolonging treatment are:
1. Your heart rate will get faster and faster and may go into an irregular rhythm, causing you to have a stroke,
2. your bones may develop osteoporosis, and
3. your body is producing antibodies to your thyroid, which will eventually destroy it and cause you to have an under active thyroid.

If you want natural, an underactive or surgically removed thyroid is better. You take hormones that your body produces naturally, but you may have to take these for the rest of your life. This is what my doctor recommended if I want to get pregnant, as the medication may be harmful to the baby but the hormones will not.

2008-02-18 04:01:08 by Kim S

Another Joe, While Recovering from Lung and Hip Cancer (Lipposarcoma) and given a grim prognosis with no hope to recover. After a few weeks, the ...

my brother was recently diagnosed with graves disease. he is 21 years old. i need to know if there is any foods he shouldn't have if so what are they. we want him on the least medications as possible because we believe in natural remedies.

Graves disease is a thyroid disorder characterized by goiter, exophthalmos, "orange-peel" skin, and hyperthyroidism. It is caused by an antibody-mediated auto-immune reaction, but the trigger for this reaction is still unknown. It is the most common cause of hyperthyroidism in the world, and the most common cause of general thyroid enlargement in developed countries.

In some parts of Europe the term Basedow’s disease or Graves-Basedow disease is preferred to Graves' disease.

History

Graves disease owes its name to the Irish doctor Robert James Graves, who described a case of goiter with exophthalmos in 1835. However, the German Karl Adolph von Basedow independently reported the same constellation of symptoms in 1840. As a result, on the European Continent the term Basedow's disease is more common than Graves' disease.[1][2][3]

Several earlier reports exist but were not widely circulated. For example, cases of goiter with exophthalmos were published by the Italians Giuseppe Flajani and Antonio Giuseppe Testa, in 1802 and 1810 respectively.[4] Prior to these, Caleb Hillier Parry, a notable provincial physician in England of the late 18th-century (and a friend of Edward Jenner),[5] described a case in 1786. This case was not published until 1825, but still ten years ahead of Graves[6]

However, fair credit for the first description of Graves disease goes to the 12th-century Persian physician Sayyid Ismail Al-Jurjani, who noted the association of goiter and exophthalmos in his Thesaurus of the Shah of Khwarazm, the major medical dictionary of its time.[7]

[edit] Diagnosis

Graves' disease may present clinically with one of the following characteristic signs:

* goiter (an enlarged thyroid gland, sometimes detectable as a swelling in the neck)
* exophthalmos (protuberance of one or both eyes)
* a non-pitting edema with thickening of the skin, described as "peau d'orange" or "orange peel", usually found on the lower extremities
* fatigue, weight loss with increased appetite, and other symptoms of hyperthyroidism

The two signs that are truly diagnostic of Graves' disease (i.e. not seen in other hyperthyroid conditions) are exophthalmos and nonpitting edema. Goiter, which is caused by an enlarged thyroid gland, can be present with other forms of hyperthyroidism, although Graves' disease is the most common cause. A large goiter is visible to the naked eye, but a smaller goiter may not be clinically detectable, though X-rays or ultrasound can assist in detecting it.

Another sign of Graves' disease is hyperthyroidism, i.e. over-production of the thyroid hormones T3 and T4. Although, hypothyroidism has also been associated and may be the causating factor in some patients. Hyperthyroidism can be confirmed by measuring elevated blood levels levels of free (unbound) T3 and T4. Other useful laboratory measurements include thyroid-stimulating hormone (TSH, low in Graves' disease due to negative feedback from the elevated T3 and T4), and protein-bound iodine (elevated). Thyroid-stimulating antibodies may also be detected serologically.

Definitive diagnosis requires a biopsy.

[edit] Other Graves' Disease Symptoms

Some of the most typical symptoms of Graves' Disease are the following:

* Palpitations
* Tachycardia (rapid heart rate: 100-120 beats per minute, or higher)
* Arrhythmia (irregular heart beat)
* Raised blood pressure (Hypertension)
* Tremor (usually fine shaking eg. hands)
* Excessive sweating
* Heat intolerance
* Increased appetite
* Unexplained weight loss despite increased appetite
* Shortness of breath
* Muscle weakness (especially in the large muscles of the arms and legs) and degeneration
* Diminished/Changed sex drive
* Insomnia (inability to get enough sleep)
* Increased energy
* Fatigue
* Mental impairment, memory lapses, diminished attention span
* Decreased concentration
* Nervousness, agitation
* Irritability
* Restlessness
* Erratic behavior
* Emotional lability
* Brittle nails
* Abnormal breast enlargement (men)
* Goiter (enlarged thyroid gland)
* Protruding eyeballs (Graves' disease only
* Double vision
* Eye pain, irritation, or the feeling of grit or sand in the eyes
* Swelling or redness of eyes or eyelids/eyelid retraction
* Sensitivity to light
* Decrease in menstrual periods (oligomenorrhea), Irregular and scant menstrual flow (Amenorrhea)
* Difficulty conceiving/infertility/recurrent miscarriage
* Hair loss
* Itchy skin, hives
* Chronic sinus infections
* Lumpy, reddish skin of the lower legs (pretibial myxedema)
* Smooth, velvety skin
* Increased bowel movements or Diarrhea

[edit] Incidence and epidemiology

The disease occurs most frequently in women (7:1 compared to men). It occurs most often in middle age (most commonly in the third to fifth decades of life), but is not uncommon in adolescents, during pregnancy, at the time of menopause and in people over age 50. There is a marked family preponderance, which has led to speculation that there may be a genetic component. To date, no clear genetic defect has been found that would point at a monogenic cause. Tissue behind the eye can become swollen or fibrous, causing the characteristic symptom of bulging eyes.

[edit] Pathophysiology

Graves' disease is an autoimmune disorder, in which the body produces antibodies to the receptor for Thyroid-stimulating hormone (TSH). (Antibodies to thyroglobulin and to the thyroid hormones T3 and T4 may also be produced.) This is an example of a type II hypersensitivity.

These antibodies cause hyperthyroidism because they bind to the TSH receptor and chronically stimulate it. The TSH receptor is expressed on the follicular cells of the thyroid gland (the cells that produce thyroid hormone), and the result of chronic stimulation is an abnormally high production of T3 and T4. This in turn causes the clinical symptoms of hyperthyroidism, and the enlargement of the thyroid gland visible as goiter.

The infiltrative exophthalmos that is frequently encountered has been explained by postulating that the thyroid gland and the extraocular muscles share a common antigen which is recognized by the antibodies. Antibodies binding to the extraocular muscles would cause swelling behind the eyeball.

The "orange peel" skin has been explained by the infiltration of antibodies under the skin, causing an inflammatory reaction and subsequent fibrous plaques.

There are 3 types of autoantibodies to the TSH receptor currently recognized:

* TSI, Thyroid stimulating immunoglobulins: these antibodies (mainly IgG) act as LATS (Long Acting Thyroid Stimulants), activating the cells in a longer and slower way than TSH, leading to an elevated production of thyroid hormone.

* TGI, Thyroid growth immunoglobulins: these antibodies bind directly to the TSH receptor and have been implicated in the growth of thyroid follicles.

* TBII, Thyroid Bind Inhibiting Inmunoglobulins: these antibodies inhibit the normal union of TSH with its receptor. By doing this, several other antibodies that normally would inhibit TSH function will actually act as if TSH itself was binding to its receptor, thus inducing thyroid function.

[edit] Etiology

The trigger for auto-antibody production is not known. There appears to be a genetic predisposition for Graves' disease, suggesting that some people are more prone than others to develop TSH receptor activating antibodies due to a genetic cause. HLA DR (especially DR3) appears to play a significant role.[8]

Since Graves' disease is an autoimmune disease which appears suddenly, often quite late in life, it is thought that a viral or bacterial infection may trigger antibodies which cross-react with the human TSH receptor (a phenomenon known as antigenic mimicry, also seen in some cases of type I diabetes).

One possible culprit is the bacterium Yersinia enterocolitica (a cousin of Yersinia pestis, the agent of bubonic plague). However, although there is indirect evidence for the structural similarity between the bacteria and the human thyrotropin receptor, direct causative evidence is limited.[8] Yersinia seems not to be a major cause of this disease, although it may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals.[9] It has also been suggested that Y. enterocolitica infection is not the cause of auto-immune thyroid disease, but rather is only an associated condition; with both having a shared inherited susceptibility.[10] More recently the role for Y. enterocolitica has been disputed.[11]

The ocular manifestations of Graves disease are more common in smokers and tend to worsen (or develop for the first time) following radioiodine treatment of the thyroid condition. Thus, they are not caused by hyperthyroidism per se; this common misperception may result from the fact that hyperthyroidism from other causes may cause eyelid retraction or eyelid lag (so-called hyperthyroid stare) which can be confused with the general appearance of proptosis/exophthalmos, despite the fact that the globes do not actually protrude in other causes of hyperthyroidism. Also, both conditions (globe protrusion and hyperthyroid lid retraction) may exist at the same time in the hyperthyroid patient with Graves disease.

[edit] Treatment

Medical treatment of Graves' disease includes antithyroid drugs, radioactive iodine and thyroidectomy (surgical excision of the gland).

Treatment of the hyperthyroidism of Graves-Basedow disease may be with medications such as methimazole or propylthiouracil (PTU), which reduce the production of thyroid hormone, or with radioactive iodine. Surgical removal of the thyroid is another option, but still requires preoperative treatment with methimazole or PTU. This is done to render the patient "euthyroid" (i.e. normothyroid) before the surgery since operating on a frankly hyperthyroid patient is dangerous. Therapy with radioactive iodine (I-131) is the most common treatment in the United States and in many other parts of the world. Thyroid blocking drugs and/or surgical thyroid removal is used more often than radioactive iodine as definitive treatment in Japan, perhaps because of general fear of radioactivity among many Japanese.

The development of radioactive iodine (I-131) in the early 1940s at the Mallinckrodt General Clinical Research Center and its widespread adoption as treatment for Graves' Disease has led to a progressive reduction in the use of surgical thyroidectomy for this problem. In general, RAI therapy is effective, less expensive, and avoids the small but definite risks of surgery. Treatment with antithyroid medications must be given for six months to two years, in order to be effective. Even then, upon cessation of the drugs, the hyperthyroid state may recur. Side effects of the antithyroid medications include a potentially fatal reduction in the level of white blood cells.

[edit] Antithyroid drugs

The main antithyroid drugs are methimazole (US), carbimazole (UK) and propylthiouracil (PTU). These drugs block the binding of iodine and coupling of iodotyrosines. The most dangerous side-effect is agranulocytosis (1/250, more in PTU); this is an idiosyncratic reaction which does not stop on cessation of drug). Others include granulocytopenia (dose dependent, which improves on cessation of the drug) and aplastic anemia. Patients on these medications should see a doctor if they develop sore throat or fever. The most common side effects are rash and peripheral neuritis. These drugs also cross the placenta and are secreted in breast milk.

[edit] Radioiodine

This modality is suitable for most patients, although some prefer to use it mainly for older patients. Indications for radioiodine are: failed medical therapy or surgery and where medical or surgical therapy are contraindicated.

Contraindications to RAI are pregnancy (absolute), ophthalmopathy (relative- it can aggravate thyroid eye disease), solitary nodules. Disadvantages of this treatment are a high incidence of hypothyroidism (up to 80%) requiring hormone supplementation. It acts slowly and has a relapse rate that depends on the dose administered.

[edit] Surgery

This modality is suitable for young patients and pregnant patients. Indications are: a large goiter (especially when compressing the trachea), suspicious nodules or suspected cancer (to pathologically examine the thyroid) and patients with ophthalmopathy.

Both bilateral subtotal thyroidectomy and the Hartley-Dunhill procedure (hemithyroidectomy on 1 side and partial lobectomy on other side) are possible.

Advantages are: immediate cure and potential removal of carcinoma. Its risks are injury of the recurrent laryngeal nerve, hypoparathyroidism (due to removal of the parathyroid glands), hematoma (which can be life-threatening if it compresses the trachea) and scarring.

[edit] Eye disease

Thyroid Eye Disease (TED) is one of the most typical symptom of Graves' Disease- also called "Graves' ophthalmopathy". Thyroid eye disease is an inflammatory condition which affects the orbital contents including the extraocular muscles and orbital fat. It is almost always associated with Graves' disease (GD) but may rarely be seen in Hashimoto's thyroiditis, primary hypothyroidism, or thyroid cancer. The ocular manifestations of TED include soft tissue inflammation, eyelid retraction, proptosis, corneal exposure, and optic nerve compression. The signs and symptoms of the disease are characteristic. These include lid retraction, lid lag, and a delay in the downward excursion of the upper eyelid in down gaze that is specific to TED.

* For mild disease - artificial tears, steroid eyedrops, oral steroids (to reduce chemosis)
* For moderate disease - lateral tarsorrhaphy
* For severe disease - orbital decompression or retro-orbital radiation

[edit] No treatment

If left untreated, more serious complications could result, including birth defects in pregnancy, increased risk of a miscarriage, and in extreme cases, death. Graves-Basedow disease is often accompanied by an increase in heart rate, which may lead to further heart complications. If the eyes are proptotic (bulging) severely enough that the lids do not close completely at night, severe dryness will occur with a very high risk of a secondary corneal infection which could lead to blindness. Pressure on the optic nerve behind the globe can lead to visual field defects and vision loss as well.

2007-05-26 10:11:08 by spiratic 1

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I don't like being a guinni pig,I think I should take natural remedies rather than other prescriptions. Plus not to mention the doctor bills, I can't afford. What would you do ?

Graves' Disease is a type of autoimmune disease that causes over-activity of the thyroid gland, causing hyperthyroidism. This over-activity is also sometimes called "toxic diffuse goiter." The thyroid gland helps set the rate of metabolism, which is the rate at which the body uses energy. When the thyroid is too active, it makes more thyroid hormones than the body needs. High levels of thyroid hormones can cause side effects such as weight loss, rapid heart rate and nervousness. This is an uncommon disease that affects 2 percent of all women at some time in their lives.
These are the most common symptoms of Graves’ Disease and hyperthyroidism:
--trouble sleeping
--fatigue
--trouble getting pregnant
--frequent bowel movements
--irritability
--weight loss without dieting
--heat sensitivity
--increased sweating
--muscular weakness
--changes in vision or how your eyes look
--lighter menstrual flow
--rapid heart beat
--hand tremors
Graves’ Disease is the only kind of hyperthyroidism that is associated with swelling of the tissue around the eyes and bulging of the eyes. And rare cases, patients will develop a lumpy reddish thickening of the skin in front of the shins called pretibial myxedema. This skin condition is usually painless. The symptoms of this disease can occur slowly or very suddenly and are sometimes confused with other medical problems. Women can also have Graves’ Disease and have no visible symptoms at all.
Graves' disease can be caused by a group of different factors that come together to cause thyroid problems, including heredity, your body's immune system, your age, sex hormones, and possibly stress.
There are three treatments for Graves' Disease:
--Medicine. There are some medicines called antithyroid drugs that can lower the amount of thyroid hormones made by the thyroid, causing it to make, normal levels. A doctor must give these medicines to you. Some patients who take an acute thyroid drug for 1 to 2 years have a remission from Graves’ disease; their thyroid function may remain normal even without medication.
--Radioactive iodine. The radioactive iodine damages thyroid cells, shrinking and eventually destroying the thyroid gland in order to reduce hormone levels. Like surgery, this condition usually leads to hypothyroidism, so that thyroid hormone supplement medication is needed for the rest of the patient's life.
--Surgery. All of the thyroid gland will be removed. In most cases, people who have surgery for Graves' Disease will develop an under-active thyroid (hypothyroidism, the opposite of hyperthyroidism), and will have to take thyroid replacement hormones for the rest of their lives.
After a diagnosis is made and a treatment is chosen, you should return to your doctor for regular follow-up visits every year to make sure that your thyroid levels are normal and for adjustments in your medicine dose if need be. (It may take some time before your levels are accurate...even if you get it taken out, you will still need medication to "fake" your body into thinking it has a thyroid)
NOW READ THIS!! If left untreated, Graves’ Disease can lead to heart problems and problems in pregnancy, and an increased risk of a miscarriage. Severe, untreated Graves’ Disease can be fatal. Thyrotoxic storm is a rare life-threatening condition that develops in cases of untreated hyperthyroidism. It is usually brought on by an acute stress, such as trauma surgery or infection. Symptoms are severe, with a pounding heart, sweating, restlessness, shaking, diarrhea, change in consciousness, agitation and confusion. Congestive heart failure can develop rapidly and lead to death.

You can find out more information about Graves' Disease by contacting the National Women's Health Information Center (800-994-9662) or the following organizations:

Graves’ Disease Foundation of America
P.O. Box 8387
Fleming Island, FL 32006
Internet address: http://www.ngdf.org

The American Thyroid Association
6066 Leesburg Pike, Suite 550
Falls Church, Virginia 22041
phone: 703 998-8890
fax: 703 998-8893
e-mail: admin@thyroid.org
Internet address: http://www.thyroid.org

Thyroid Foundation of America, Inc.
One Longfellow Place
Suite 1518
Boston, MA 02114
phone (toll-free): 800 832-8321
phone: 617 534-1500
fax: 617 534-1515
e-mail: info@allthyroid.org
Internet address: http://www.allthyroid.org

And, if you're interested, here's some info about me, and for anyone else who may come across your question & needs more information about thyroid problems:
I have low thyroid. If you have low thyroid...here's a great question to answer: Can you see the floor of your house? That was what was asked of me at one point, and to my amazement, the answer was no!
Anyway, the signs are:fatigue and lack of energy. Women suffering from underactive thyroid experience heavier menstrual periods. Sluggishness and forgetfulness are symptoms of underactive thyroid problem. Other symptoms of this thyroid disorder are dry skin and hair and constipation.
If you have high thyroid, or an overactive one, the signs are: increased body metabolism. This is followed by weight loss and excessive warmth and sweating. Persons suffering from overactive thyroid experience trembling hands, irritability and rapid heartbeat or palpitations. Women with overactive thyroid or hyperthyroidism may experience shorter or lighter menstrual periods.
I take medication, and sadly will have to take 1 pill everyday for the rest of my life. There's a blood check that they will do to see if you have low or high. Again, as I mentioned before, it may take some ups & downs until the medicine gets where it needs to be for you. I hope i've helped you!!

2006-06-19 02:41:54 by tinatomtkt