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.
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.
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. Prior to these, Caleb Hillier Parry, a notable provincial physician in England of the late 18th-century (and a friend of Edward Jenner), described a case in 1786. This case was not published until 1825, but still ten years ahead of Graves
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.
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.
 Other Graves' Disease Symptoms
Some of the most typical symptoms of Graves' Disease are the following:
* 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
* Mental impairment, memory lapses, diminished attention span
* Decreased concentration
* Nervousness, agitation
* 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
 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.
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.
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.
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. 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. 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. More recently the role for Y. enterocolitica has been disputed.
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.
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.
 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.
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.
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.
 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
 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. (+ info
I just found out my husband is having an affair with a woman that has Graves Disease. Is it possible for him to transfer that to me? I am sure she is alright in all other ways but know nothing about the Disease.
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 a common disease that affects 2 percent of all women at some time in their lives. Graves’ Disease also tends to affect women between the ages of 20 and 40, although it occurs in infants, children, and the elderly.
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.
You can inherit a greater likelihood to have hyperthyroidism, which means that you may develop Graves' disease at some time during your life.
Most autoimmune diseases occur in women, and most often during their childbearing years. Some of these diseases also affect African American, American Indian, and Latina women more than white women. These diseases tend to run in families, so your genes, along with the way your immune system responds to certain triggers or things in the environment, affect your chances of getting one of these diseases. If you think you may have an autoimmune disease, ask your family members if they have had symptoms .
but you cant catch it through sex, (+ info
I was diagnosed with Graves 7 years ago. I had radioactive iodine and now take synthroid. I don't feel beeter. I am always tired and I can not lose weight. Help any ideas
I take the same medication and got the radioactive iodine thing done too. If I felt tired alot I would go back and tell your doctor, maybe he needs to adjust the dosage, or find out if there are any other reasons why you may be tired. It does sound like maybe the dosage is too low. Also I read in the pamplet that comes with the medication to take on an empty stomach or it may not be as effective. I didn't know that and have been taking mine with meals. See the Doc! (+ info
My mother has graves disease which has affected the eyes but has been turned down the operation?
Graves disease affects the thyroid and in result has made the eyes bigger. We can clearly see they need surgery to correct them but the doctors have said its cosmetic and will not do the operation. Is there any type of procedure to appeal for this? Also any web site available, informing what wright's we have.
Thank you for your time.
Oh we live in the UK aswell.
Go to a naturopath!!
I was diagnosed with Hashimoto thyroiditis, adrenal fatigue & gluten/wheat/dairy intolerance. The fatigue & achiness were unbearable, as I felt like walking death! Thank God, a naturopath did a saliva test to check my hormone levels & introduced me to plant based bioidentical hormones. (+ info
What can a person with Graves Disease do to lose weight?
I am 16 and i have Graves Disease (hyperactive thyroid) and when i was first diagnoised, i was put on medication that made me gain 30 pounds in like less than 3 months. Now i am currently 40 pounds heaver than i was. I would like to lose at least 20 pounds. How can i do it the fastest way?
Im sorry to hear that! I would go on a low carb diet or weight watchers. Both of these have worked for my friends. I think w/ low carb you will lose weight the fastest. good luck! (+ info
What is an actual, easy to understand definition of graves disease?
I am a teen and when i tell people i have graves disease they never know what it is. Like yesterday, I went for an appointment and my crush asked my friends where I was and the dears they are told him I was at the hospital! And I didn't know how to explain to him my condition. Thanks in advance!
Graves' disease is the most common form of hyperthyroidism. It occurs when your immune system mistakenly attacks your thyroid gland and causes it to overproduce the hormone thyroxine.
The abnormal immune response can affect the tissue behind your eyes as well as parts of your skin. The higher thyroxine level in Graves' disease can greatly increase your body's metabolic rate, leading to host of health problems.
Graves' disease is rarely life-threatening. Although it may develop at any age and in either men or women, Graves' disease is more common in women and usually begins after age 20.
There's no way to stop your immune system from attacking your thyroid gland, but treatments for Graves' disease can ease symptoms and decrease the production of thyroxine. (+ info
How long can you go with Graves Disease without being treated?
I went to a specialist last week - she diagnosed me with Graves Disease. It makes sense, I have all the symptoms. I am not happy with the office's response rate. The doctor told me I should get the radioiodine this week and no one is calling me back. There is another endo in the area, but they are booked through April. Can I wait that long?
You should not. Find another doctor, one who is actually concerned for your health. The first doctor should have at the very least given you a beta blocker. A beta blocker is a temporary, emergency treatment for Grave's disease until the treatment kicks in. You should also have been given an anti thyroid drug. In the US, they give you methimizole.
Once you have the methimizole, you don't need radioactive iodine. RAI is not a cure for Grave's disease. It only treats one symptom of Graves disease - the hyperthyroidism. Plus it gives you an additional disease - hypothyroidism. If you don't want this, don't have the radioactive iodine.
So see another doctor. Any old GP will do, if they are willing. You don't actually need an endo. As long as you can get the right blood tests, (free T3 and free T4) and methimizole, you will be fine. (+ info
Does anyone know of any alternative methods for Graves disease? Has this worked for anyone?
I have Graves disease, my doctor is really rude and won't answer questions for me. I started this diet and I think that it is helping but I am still learning about ways to control the hyperthyroidism.
I'm sorry to hear you have Graves disease; I have Hashimoto's...the opposite autoimmune disease.
Before trying any remedies, though, I think you'd be wise to read a little about it first from these sites:
Good luck! (+ info
how much money does it cost for radioactive iodine for graves disease?
i have graves disease. i want to know how much money it costs for the radioactive iodine.
it usually costs a lot and after the medication you gotta have maintainance as well...check out the philippines (+ info
What is a biochemical aspect of Graves' disease?
I am doing a presentation in biochemistry on Graves' disease and I need to pick something out that deals with Graves' disease to focus on.
Biochemical aspects would be the mechanics of the disease and the effects the disease has on the body. This should be sufficient information to point you int he right direction and enable you to continue your research. (+ info
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