The Difference Between Euthyroid and Remission Explained
Protect Your Thyroid from Radiation and Iodine Exposure During Medical Imaging
By Emily Lyth on Sunday, January 18, 2015 at 10:47 PM
To diagnose hyperthyroidism/Graves’, most doctors rely on testing the following:
TSH- thyroid stimulating hormone
Free T3- Free Triiodothyronine
Free T4- Free Thyroxine
TRAb- TSH receptor antibody
TSI- thyroid stimulating immunoglobulin
To understand how to interpret these levels, you must first have a basic understanding of how the thyroid works. The thyroid is essentially controlled by the pituitary gland. The pituitary gland releases a hormone called TSH (thyroid stimulating hormone). TSH is what signals the thyroid to produce T4. T4 is considered an inactive form of thyroid hormone because it is converted to T3 (an active form of thyroid hormone) for the body to utilize. The thyroid produces very little T3 on its own, as most of the T4 it produces is converted to T3 in the liver, GI tract, and various other locations throughout the body. Once T4 has been converted into T3, the T3 serves as a messenger that signals back to the pituitary gland that the thyroid received the pituitary gland’s message. When the pituitary gland receives this message, it regulates the production of TSH. This feedback loop between the pituitary gland & the thyroid is what regulates TSH, T3 and T4 production. Please note that T3 and T4 can both be measured as Free or Total. Free values are a measure of the unbound hormone in the bloodstream; this means they are readily available for use. Total values measure both the bound & unbound hormone levels. Free values can usually provide a more accurate measure of thyroid hormone levels. So what does all this have to do with your thyroid labs?
Well, when you have Graves’, you also have antibodies (TRAb/TSI). These antibodies stimulate the thyroid in a way that mimics TSH while they also block TSH from binding to the thyroid. In other words, these antibodies interfere with the feedback loop between the pituitary gland & the thyroid that is described above. So rather than TSH instructing the thyroid to produce T4 as it should, the thyroid is instructed to produce T4 through the antibody’s stimulation, which is then converted to T3. As stated previously, this T3 goes on to signal the pituitary gland that TSH can be suppressed. As the disease progresses and the thyroid becomes overstimulated by the antibodies, T4 and T3 levels continue to rise. The overwhelming amount of T3 caused by antibody stimulation deceives the pituitary gland into thinking that it’s producing too much TSH. In an effort to resolve this problem, the pituitary gland begins producing less and less TSH.
That being said, by the time most Graves’ patients are displaying symptoms & diagnosed, their TSH is usually very low (or so low it’s not even measurable at all) while their Free T3 & Free T4 values are elevated. Antibody levels (TRAb/TSI) are also detectable or elevated. Testing antibody levels is incredibly important to confirm a Graves’ diagnosis because there are other causes of hyperthyroidism, such as thyroid nodules, that can stimulate the thyroid and cause excess hormone production.
In order to interpret what your lab results mean, you must have your lab values along with the reference ranges used by your lab; your lab values mean nothing without the reference range. Always ask for a copy of your lab results and hang on to them!
In cases of extreme hyperthyroidism, TSH will fall below the range provided while Free T3 and Free T4 will exceed the range provided. In other words, low TSH in combination with high Free T3 and high Free T4 are indicative of hyperthyroidism. The lower your TSH and the higher your Free T3 and Free T4, the more extreme your hyperthyroidism is. Similarly, a TSH that is high in combination with a low Free T3 and a low Free T4 indicates hypothyroidism. Graves’ patients who are kept on a high initial dose of anti-thyroid drug for too long will typically swing from being hyper to hypo (or somewhere in the normal range but close to hypo) because they are over-medicated. This resolves itself once the dose of anti-thyroid is adjusted.
TSH Free T3 Free T4 Interpretation
Low High High Hyperthyroidism
High Low Low Hypothyroidism
It’s important to understand that TSH can take quite some time to respond to treatment. It’s not uncommon for TSH to remain close to zero for an extended amount of time. Free T3 and Free T4 are a much clearer representation of your thyroid’s current health.
It’s also important to note that just because your thyroid lab results fall within the reference range does not mean they are optimal. There’s a difference between normal levels and optimal levels. It is generally accepted that optimal Free T4 values lie within the upper half of the reference range while optimal Free T3 values lie within the upper quarter of the reference range. If your levels are within the normal range but you feel something is off, it could very well be because your levels are normal but they’re not optimal. The reference range is so broad for thyroid levels that what one person finds optimal may not be optimal for someone else. Finding where your Free T3 and Free T4 levels are optimal so you feel your best can take some time, patience, and dosage adjustments. Keeping a journal to track your medications, doses, and symptoms can be very helpful in determining your own optimal levels.
Helpful links:
http://endocrine.niddk.nih.gov/pubs/thyroidtests/
http://www.drrind.com/therapies/thyroid-scale
Knowledge is power!
MELODY OLSEN·WEDNESDAY, SEPTEMBER 21, 2016·
For our members in the UK who are having difficulty getting the tests they need/getting them at a reasonable price, one of our members found this service: Blue Horizon Medicals do a finger prick test for TSH and FT4 called the Basic Thyroid Profile for £39, and the Intermediate Thyroid Profile includes TSH, FT4 and FT3 for £49. There are other groupings of thyroid blood tests and antibodies on their website. You get sent little lancets to stab the end of one of your fingers, then you just squeeze enough blood out of your finger to fill a small tube. It’s done by post and they email you the results within a couple of days. According to group member Rona Millington, they have been really reliable with her and she once had the NHS test and their test done a few days apart to see if the results were the same and they were. The website is:
BLUEHORIZONMEDICALS.CO.UK
KATHRYN CLEMENS·MONDAY, SEPTEMBER 19, 2016·
If you feel awful and your doctor is only testing TSH or putting too much importance on TSH, this is why! TSH is a pituitary hormone that tells the thyroid how much thyroid hormone it needs to make. So why is TSH not a good indicator of progress with Graves? Because our antibodies alter it, that’s why.
TRab antibodies (Thyrotropin Receptor Antibodies) the Graves antibodies actually attack your TSH and alter it. So when your pituitary gland tries to tell your thyroid gland enough thyroid has been made the TRab intercept that message and change it to say, make more, make more, make more! So your already overactive thyroid thinks it must make even more thyroid hormone. It’s a vicious, perpetuating cycle.This is why we cannot follow TSH when managing Graves in the first stages of treatment and recovery. For many TSH may not respond for months to years. TSH will not respond properly until antibodies get low enough to stop jacking with it.Many doctors think over medicating with anti thyroid meds will force TSH to respond. And eventually it will but this is a false victory that leaves the patient hypo and feeling worse than when hyper. This is not a good solution!!Instead we manage Graves by Free T4 and Free T3. These are the ACTUAL thyroid hormones and they are not directly stimulated by Graves antibodies. The Free means they are free and unbound hormone ready and available for your body to utilize. Manage your Graves Disease by getting your FT4 and FT3 in optimal range and you’ll feel much much better!! You’ll also be lowering your antibodies as you’re feeling better.If your doctor will only test TSH he/she is not Graves savvy. If your doc refuses to test FT4 and FT3, find another doctor!!!
MELODY OLSEN·THURSDAY, SEPTEMBER 15, 2016·
Cod liver oil is a source of properly balanced vitamin A and hormone D, plus EPA and DHA omegas. Following is some information regarding iodine content of two brands of cod liver oil.
One of the members of our group called Nordic Naturals and NutraPro International to ask about the iodine content of their Arctic cod liver oil. She spoke to a nutritionist who was also a chemist. NutraPro has NO iodine in it! The cold press process lets the pure fat of the CLO rise to the top (with its natural fat soluble vitamins of A and D), while the proteins grab any heavier minerals and they get weighted down to the bottom of the container. The iodine is found in the blood steam and in the muscles of the cod fish and not in the pure fat of the oil.
She also spoke to Nordic Naturals about their CLO. They say that their CLO has 1/2 – 1.0 mcg of iodine per serving a day of 1 tsp of CLO. They say that they label it this way due to the people who are sensitive to the iodine content of dyes for CT’s and other imaging scans. This is good news, so we can still take cod liver oil for the benefits of the EPA/DHA fatty acids and the non-synthetic vitamins A and hormone D and not worry about excess iodine.
MELODY OLSEN·WEDNESDAY, SEPTEMBER 7, 2016·
Highlights from 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and other causes of Thyrotoxicosis
http://online.liebertpub.com/doi/pdfplus/10.1089/thy.2016.0229
“While it might be anticipated that the severity of thyrotoxic symptoms is proportional to the elevation in the serum levels of free T4 and T3, in one small study of 25 patients with GD, the Hyperthyroid Symptom Scale did not strongly correlate with free T4 or T3 and was inversely correlated with age (28). The importance of age as a determinant of the prevalence and severity of hyperthyroid symptoms has been recently confirmed (30).”
“Goiter size, obstructive symptoms, and the severity of Graves’ orbitopathy (GO), the inflammatory disease that develops in the orbit in association with autoimmune thyroid disorders, can be discordant with the degree of hyperthyroidism or hyperthyroid symptoms.”
“Ingestion of high doses of biotin may cause spurious results in assays that utilize a steptavidinbiotin separation technique (41,42). In immunometric assays, frequently used to measure TSH, excess biotin displaces biotinylated antibodies and causes spuriously low results, while in competitive binding assays, frequently used to measure free T4, excess biotin competes with biotinylated analogue and results in falsely high results. Patients taking high doses of biotin or supplements containing biotin, who have elevated T4 and suppressed TSH should stop taking biotin and have repeat measurements at least 2 days later.”
Diagnostic Testing
“In a study using a model of a theoretical population of 100,000 enrollees in a managed care organization in the United States, the use of TRAb measurements to diagnose GD compared to RAIU measurements reduced costs by 47% and resulted in a 46% quicker diagnosis (45).”
“Uptake measurements are indicated when the diagnosis is in question (except during pregnancy and usually during lactation (see section [T4]) and distinguishes causes of thyrotoxicosis having elevated or normal uptake over the thyroid gland from those with near-absent uptake (Table 3).”
“A thyroid scan should be obtained if the clinical presentation suggests a toxic adenoma or toxic multinodular goiter. The pattern of RAIU in GD is diffuse unless there are coexistent nodules or fibrosis. The pattern of uptake in a patient with a single TA generally shows focal uptake in the adenoma with suppressed uptake in the surrounding and contralateral thyroid tissue. The image in TMNG demonstrates multiple areas of focal increased and suppressed uptake. If autonomy is extensive, the image may be difficult to distinguish from that of GD (46). Additionally, GD and non-toxic nodular goiter may coincide resulting in positive TRAb levels and a nodular ultrasound or heterogeneous uptake images (47).”
“Where expertise is available, ultrasonography with color Doppler flow can distinguish thyroid hyperactivity (increased flow) from destructive thyroiditis (48).”
“The ratio of total T3 to total T4 can also be useful in assessing the etiology of thyrotoxicosis when scintigraphy is contraindicated. Because a hyperactive gland produces more T3 than T4, T3 will be elevated above the upper limit of normal more than T4 in thyrotoxicosis caused by hyperthyroidism, whereas T4 is elevated more than T3 in thyrotoxicosis caused by thyroiditis (50); in one study the ratio of total T3/total T4 (ng/mcg) was >20 in GD and toxic nodular goiter, and <20 in painless or postpartum thyroiditis (51). A high T4 to T3 ratio may be seen in thyrotoxicosis factitia (from exogenous levothyroxine).”
“The choice of initial diagnostic testing depends on cost, availability, and local expertise. TRAb is cost-effective because if it is positive it confirms the diagnosis of the most common cause of thyrotoxicosis, but if negative it does not distinguish among other etiologies, and it can be negative in very mild GD. If third generation TRAb assays are not readily available, RAIU is preferred for initial testing. Diagnostic testing may be influenced by the choice of therapy (see Section [C]). For example, measuring TRAb in a patient with GD who plans on taking methimazole (MMI) with the hope of achieving a remission will provide a baseline measurement for disease activity. Obtaining a RAIU in a patient who prefers radioactive iodine treatment will provide both diagnostic information and facilitate the calculation of the radioactive iodine dose (see Section [D2]).”
“There are two methods for measuring TRAb (55). Third-generation TSH binding inhibition immunoglobulin (TBII) assays are competition-based assays which measure inhibition of binding of a labeled monoclonal anti-human TSHR antibody (or labeled TSH) to recombinant TSHR. Bioassays for thyroid stimulating immunoglobulin (TSI) measure the ability of TSHR autoantibodies or TSH to increase intracellular cAMP levels directly or indirectly, e.g. from Chinese hamster ovary cells transfected with hTSHR. Such assays detect blocking as well as neutral and stimulating immunoglobulins. The newer TRAb assays are positive in 96% of patients with GD (56). Older TSI assays were more specific but less sensitive than TBII assays. In the setting of thyrotoxicosis, third generation TBII assays have a sensitivity of 97% and a specificity of 99% (57).”
Treatment with ATDs
“The treatment itself might have a beneficial immunosuppressive role, either to primarily decrease thyroid specific autoimmunity, or secondarily, by ameliorating the hyperthyroid state, which may restore the dysregulated immune system back to normal (111). In fact, the rate of remission with ATD therapy is much higher (112) than the historical rates of spontaneous remission (113).”
“ The task force suggests the following as a rough guide to initial MMI daily dosing: 5-10 mg if free T4 is 1-1.5 times the upper limit of normal (ULN); 10-20 mg for free T4 1.5-2 times the ULN; 30-40 mg for free T4 2-3 times the ULN. These rough guidelines should be tailored to the individual patient, incorporating additional information on symptoms, gland size and total T3 levels where relevant. Serum T3 levels are important to monitor initially, as some patients normalize their free T4 levels with MMI but have persistently elevated serum T3, indicating continuing thyrotoxicosis (117)”
“Baseline blood tests to aid in the interpretation of future laboratory values should be considered before initiating ATD therapy. This is suggested in part because low white cell counts are common in patients with GD and in African Americans (10% of whom have a neutrophil count under 2000 (148)), and abnormal liver enzymes are frequently seen in patients with thyrotoxicosis (149).”
“An assessment of serum free T4 and total T3 should be obtained about 2 to 6 weeks after initiation of therapy, depending on the severity of the thyrotoxicosis, and the dose of medication adjusted accordingly. Serum T3 should be monitored because the serum free T4 levels may normalize despite persistent elevation of serum total T3. Serum TSH may remain suppressed for several months after starting therapy and is therefore not a good parameter for monitoring therapy early in the course”
“Once the patient is euthyroid, the dose of MMI can usually be decreased by 30-50%, and biochemical testing repeated in 4-6 weeks. Once euthyroid levels are achieved with the minimal dose of medication, clinical and laboratory evaluation can be undertaken at intervals of 2–3 months. If a patient is receiving long-term MMI (> 18 months), this interval can be increased to 6 months.”
Remission
“Measurement of TRAb levels prior to stopping ATD therapy is suggested, as it aids in predicting which patients can be weaned from the medication, with normal levels indicating greater chance for remission.”
“A patient is considered to be in remission if they have had a normal serum TSH, free T4, and total T3 for 1 year after discontinuation of ATD therapy. The remission rate varies considerably between geographical areas. In earlier studies in the United States, about 20%–30% of patients were reported to have a lasting remission after 12–18 months of medication, (59), but more recent data are not available. The remission rate may be higher in Europe and Japan; a long-term European study indicated a 50–60% remission rate after 5–6 years of treatment (163), and a study in Japan reported a 68% remission rate after 2 years of treatment (164).”
“TRAb assessment at the end of the course of ATD therapy is a useful method of dividing patients into 2 groups: one with persistent elevations who are unlikely to be in remission, and another group with low or undetectable TRAb, who have a higher probability of permanent remission (171,172). In the group with elevated TRAb, relapse rates approach 80-100%, while in the latter group, relapse rates are in the 20-30% range (171,172).”
“Patients with persistently high TRAb could continue ATD therapy (and repeat TRAb after an additional 12-18 months)…In selected patients (i.e., younger patients with mild stable disease on a low dose of MMI), long-term MMI is a reasonable alternative approach (65,173). Another study by the same author reported that MMI doses of 2.5 – 10 mg/day for a mean of 14 years were safe and effective for the control of GD in 59 patients (174). A recent retrospective analysis compared long-term outcomes (mean follow up period of 6-7 years) of patients who had relapsed after a course of ATDs, who were treated with either RAI and levothyroxine or long-term ATD therapy (175). Those patients treated with RAI (n=114) more often had persistent thyroid eye disease, continuing thyroid dysfunction, and experienced more weight gain compared to those patients receiving long-term ATD treatment (n=124). If continued MMI therapy is chosen, TRAb levels might be monitored every 1-2 years, with consideration of MMI discontinuation if TRAb levels become negative over long term follow up. For patients choosing long-term MMI therapy, monitoring of thyroid function every 4-6 months is reasonable, and patients can be seen for follow up visits every 6-12 months.”
“In patients with negative TRAb, relapses tend to occur relatively later than those that develop in patients whose MMI is stopped when TRAb is still positive (171,176), although 5% occurred within the first 2 months (167). Therefore, in this population, thyroid function testing should be monitored at 2 to 3-month intervals for the first 6 months, then at 4 to 6-month intervals for the next 6 months, then every 6 to 12 months, in order to detect relapses as early as possible…If the patient remains euthyroid for more than 1 year (i.e., they are in remission), thyroid function should be monitored at least annually, as relapses can occur years later (171), and some patients eventually become hypothyroid (179).”
Management of GD in children
“Because some children will go into remission, MMI therapy for 1 year is still considered firstline treatment for most children….When ATDs are used in children, only MMI should be used, except in exceptional circumstances.”
“MMI comes in 5 or 10 mg tablets and can be given once daily, even in patients with severe hyperthyroidism. Although many practitioners give MMI in divided doses, data in adults do not support a need for such and show that compliance with once-daily MMI therapy is superior to multiple daily doses of PTU (83% vs. 53%) (319). The MMI dose typically used is 0.2–0.5 mg/kg daily, with a range from 0.1–1.0 mg/kg daily (320-322). One approach is to prescribe the following whole tablet or quarter to half-tablet doses: infants, 1.25 mg/day; 1–5 years, 2.5–5.0 mg/day; 5–10 years, 5–10 mg/day; and 10–18 years, 10–20 mg/day. With severe clinical or biochemical hyperthyroidism, doses that are 50–100% higher than the above can be used. Although there may be a tendency to use higher rather than lower doses of MMI at treatment onset, data in adults show only modest benefit of higher doses, and only in severe thyrotoxicosis (free T4 > 7 ng/dl (0.554 pmol/L)) (115). Because most side effects of MMI are dose-related, and occur within the first 3 months of treatment (128), high doses of MMI (e.g., >30 mg for an adolescent or adult) should rarely be used initially.”
“After initiation of MMI therapy, thyroid function tests (free T4, total T3, TSH) are obtained at 2-6 weeks, the dose is adjusted if indictated, and thyroid function tests are measured again at 4-6 weeks, and then every 2–3 months once the dose is stablized. Depending on the severity of hyperthyroidism and the MMI dose, it can take several months for elevated thyroid hormone levels to fall into the normal range. Serum TSH may remain suppressed for several months after starting therapy and is therefore not a good parameter to monitor therapy early in the course.”
“Persistence of GD in children is correlated with the persistence of TRAbs. A recent study found that TRAb levels normalized after 24 months in only 18% of pediatric patients on ATDs (346). There were no data showing that there was normalization of TRAb levels when patients were on ATDs for a longer time. Therefore, it appears that TRAb levels persist longer in children than in adults (346).”
“Whereas most studies, including recent large database reports (343), show that the vast majority of patients treated for GD with ATDs do not go into remission, a recent prospective report from France shows that with prolonged ATD use, remission rates of up to 49% could be achieved. This study reported remision rates of 20%, 37%, 45%, and 49% after 4, 6, 8, and 10 years follow-up of 154 children treated with ATDs (337). The use of MMI in this group of children was associated with a very low rate of medication side effects (337). Thus, whereas many practitioners will treat for 1-2 years with MMI, these data suggest that treatment for longer periods is also reasonable, as long as side effects to medication do not occur.”
Related to Pregnancy/Nursing
“ATD therapy should be used for overt hyperthyroidism due to GD during pregnancy. PTU should be used when ATD therapy is given during the first trimester. MMI should be used when ATD therapy is started after the first trimester.”
“MMI and PTU both appear in breast milk in only small concentrations and studies of breast-fed infants of mothers taking ATDs have demonstrated normal thyroid function and subsequent normal intellectual development (109). However, because of the potential for hepatic necrosis in either mother or child from maternal PTU use, MMI is the preferred ATD in nursing mothers.”
“Women taking PTU during the 1st trimester of pregnancy according to recommendations 80, 83 or 87 may be switched to MMI at the beginning of the 2nd trimester, or they may continue PTU therapy for the remaining part of pregnancy if ATD is needed. The reason for the FDA black box warning against PTU therapy after the 1st trimester of pregnancy is the risk of PTU associated liver failure. However, even if this risk is real, the absolute risk observed in studies of US health databases was low (433,465). Similarly, a recent Danish national registry study observed one case of reversible liver failure among 1103 women treated with PTU in pregnancy (129).”
“GD during pregnancy should be treated with the lowest possible dose of ATD needed to keep the mother’s thyroid hormone levels at or slightly above the reference range for total T4 and T3 values in pregnancy (1.5 times above non-pregnant reference ranges in the 2nd and 3rd trimester), and the TSH below the reference range for pregnancy. Similarly, free T4 levels should be kept at or slightly above the upper limit of the pregnancy trimester reference range for the assay. Thyroid function should be assessed at least monthly, and the ATD dose adjusted, as required.”
“Although many patients with GD may enter remission of the autoimmune abnormality during the 2 nd half of pregnancy with a need of ATD dose reduction or withdrawal, this is not a universal phenomenon.”
“TRAb (TBII or TSI) measurement may be useful to assist in the evaluation of disease activity in a woman being treated with ATDs for GD during pregnancy (444,495). In many patients, GD gradually remits during pregnancy. Disappearance of TRAb is an indication that ATD therapy may no longer be necessary, and that its continuation may put the fetus at risk for hypothyroidism, even if the mother is euthyroid on the medication.”
“ In a prospective study of pregnant women, those with positive thyroperoxidase (TPO) antibodies in the first trimester were 27 times more likely to develop postpartum thyroiditis than were those with negative serology (507).”
“Postpartum thyroiditis must be distinguished from GD to recommend proper therapy. The postpartum surge in thyroid autoimmunity leading to postpartum thyroiditis is also associated with a 3-4 fold increase in the incidence of GD that peaks 3-12 months after delivery (456).”
“Because propranalol and metoprolol are secreted into breast milk in only very low amounts, no special monitoring is needed for breastfed infants of mothers on these medications (514).”
By Carly Becker Greco on Friday, February 26, 2016 at 2:19 PM
So far this is the only brand approved by the Group for protein shakes: Vegan Sweet Vanilla premade shake in blue tetra pak is approved
CRISTIN PHILLIPS FLANDERS·SUNDAY, AUGUST 30, 2015·
There’s been a lot of confusion regarding the iodine content of different kinds of salt. This is an attempt to clarify the conflicting data and make recommendations for individuals attempting to follow a low iodine diet.
If you want to avoid iodine *completely* you should buy a very processed grocery store salt (table salt, sea salt, kosher salt, etc.). These salts, for all intents and purposes, have had any trace minerals (including iodine) eliminated during the refining process. They will be chemically similar (with some variation in crystal size, etc.) and may or may not include an added anti-caking agent (which won’t affect iodine content) and a filler.
If you want *trace* amounts of iodine (along with other trace nutrients), you should buy either unrefined sea salt, pink Himalayan salt, or Real Salt. These all originated as sea salt and have roughly the same chemical composition. I found this breakdown for pink Himalayan salt http://themeadow.com/pages/minerals-in-himalayan-pink-salt-spectral-analysis Real Salt, according to its website http://www.realsalt.com/sea-salt/know-your-salts/, says pink Himalayan salt will have roughly the same chemical composition (sodium chloride plus 60 trace minerals) as its own and any unrefined sea salt.
This is why it’s difficult to determine the true iodine content of unprocessed salt:
According to the above breakdown, pink Himalayan salt has less than 0.1 g/kg of iodine. This translates to roughly 100,000 mcg of iodine per 2.2 pounds of salt (the daily value for iodine is 150 mcg). The point, though, is that it contains *less* than 0.1 g/kg. Therefore, we really don’t know the true iodine content of pink Himalayan salt (or, by extension, any unprocessed salt) . Since Real Salt http://www.realsalt.com/sea-salt/does-real-salt-have-the-iodine-we-need/ says it’s brand has less iodine than iodized table salt (which clocks in at .045 g/kg), we have to assume that the 0.1 g/kg estimate for pink Himalayan (and therefore all the unprocessed salts) is high and, basically, unreliable. We can assume, therefore, that pink Himalayan salt, unprocessed sea salts and Real Salt (based on the available data) have somewhere between the negligible iodine content of highly processed salts and the .045 g/kg of iodized table salts.
So, again, if you want to be assured that you are getting *no* iodine* in your salt, you would be wise to stick with a processed grocery store salt. If you want an unprocessed salt with an undetermined “trace” amount of iodine (which will still be less than standard iodized salt), you might be more comfortable with an unprocessed sea salt (such as Celtic), a pink Himalayan salt, or Real Salt.
MELODY OLSEN·FRIDAY, APRIL 15, 2016·
**Research by Val Collins
“In GD, TRAb should be tested before deciding whether methimazole can be stopped” http://www.ncbi.nlm.nih.gov/pubmed/23539719
“The relationship between TRAb negativity or positivity and remission or relapse was statistically significant” http://www.thyroid.jp/pdf/dr_prediction_of_Graves_remission.pdf **”This article is 10 years old, and since that time, better antibody tests have been developed — some are now 4th generation — that help us predict remission even better.”
“CONCLUSIONS: Relapse rates of Graves’ disease were independent of ATD regimen whether followed by l-T(4) therapy or not. Smoking, large goiter and presence of TRAb at the end of ATD therapy were strong predictors of relapse.” http://www.eje-online.org/content/147/5/583.abstract?ijkey=44914095ce0fd649838e70cba03b8ad9b33c1274&keytype2=tf_ipsecsha
Also see related article in files section: “Difference Between Euthyroid and Remission Explained”
CARLY BECKER GRECO·FRIDAY, APRIL 8, 2016·
The symptoms of Graves disease, organized by systems, are as follows:
General – Fatigue, general weakness
Dermatologic – Warm, moist, fine skin; sweating; fine hair; onycholysis; vitiligo; alopecia; pretibial myxedema
Neuromuscular – Tremors, proximal muscle weakness, easy fatigability, periodic paralysis in persons of susceptible ethnic groups
Skeletal – Back pain, increased risk for fractures
Cardiovascular – Palpitations, dyspnea on exertion, chest pain, edema
Respiratory – Dyspnea
Gastrointestinal – Increased bowel motility with increased frequency of bowel movements
Ophthalmologic – Tearing, gritty sensation in the eye, photophobia, eye pain, protruding eye, diplopia, visual loss
Renal – Polyuria, polydipsia
Hematologic – Easy bruising
Metabolic – Heat intolerance, weight loss despite increase or similar appetite, worsening diabetes control, weight gain is also possible
Endocrine/reproductive – Irregular menstrual periods, decreased menstrual volume, gynecomastia, impotence
Psychiatric – Restlessness, anxiety, irritability, insomnia
By Kathryn Clemens on Thursday, December 3, 2015 at 5:24 PM
How to split a thyroid pill without a pill splitter.
KATHRYN CLEMENS·MONDAY, AUGUST 24, 2015·
- Iodized salt, sea salt and salty foods. Because it’s hard to know which restaurants use iodized salt, you might want to avoid eating out during this time
- All dairy products (milk, sour cream, cheese, cream, yoghurt, butter, ice cream)
- Margarine
- Egg yolks
- Seafood (fish, shellfish, seaweed, kelp)
- Foods that contain carrageen, agar-agar, algin, or alginate — all of these are made from seaweed
- Many prepared and/or cured meats (ham, bacon, sausage, corned beef, etc)
- Fresh chicken or turkey with broth or additives injected
- Dried fruit
- Canned vegetables
- Commercial bakery products
- Chocolate
- Molasses
- Soy products (soy sauce, soy milk, tofu)
- Any vitamins or supplements that contain iodine
- E 127 Erythrosine — this appears in many foods or pills that are red or brown, including colas
Treatment
By Cristin Phillips Flanders on Wednesday, April 29, 2015 at 1:51 PM
Topic: GRAVES- HYPERTHYROIDISM
Title: Continued suppression of serum TSH level may be attributed to TSH receptor antibody activity as well as the severity of thyrotoxicosis and the time to recovery of thyroid hormone in treated euthyroid Graves- patients.
Authors: Chung YJ, Lee BW, Kim J-Y, Jung JH, Min Y-K, Lee M-S, Lee M-K, Kim K-W, Chung JH.
Reference: Thyroid 16: 1251-1257, 2006
Summary
Background
Serum TSH may remain suppressed for weeks or months despite normalization of serum T 4 and T 3 concentrations during antithyroid drug treatment in patients with Graves- hyperthyroidism.
Purpose
To evaluate the relationship between TSH receptor antibodies or other clinical parameters and the continued suppression of serum TSH during antithyroid drug therapy in Graves- disease.
Patients & Methods
One hundred and sixty seven patients with Graves- disease were studied. They had remained euthyroid for at least 12 months after normalization of serum T 3 and T 4 during treatment with antithyroid drugs. Initial therapy with 200-450 mg of propylthiouracil (n=137) or 15-45 mg of methimazole (n=30) resulted in normal serum T 3 and T 4 after 2.8 – 1.6 months in all patients. Antithyroid drugs with dose adjustments were continued for up to 36 months. Recovery of serum TSH was defined as a return of serum TSH to levels >0.30 mU/L. TSH receptor antibodies were measured using a first generation TBII assay: values >15% were considered positive.
Results
At the time of diagnosis, there were no differences in age, sex ratio, serum T 4 and TSH between TBII-positive (N=133) and TBII-negative (N=34) patients, but serum T 3 and I-131 uptake were higher in TBII-positive patients. The interval between onset of treatment and recovery of TSH was 8.7 – 5.9 months. This interval was positively correlated to pretreatment serum T 3 , uptake of I-131, and TBII. The interval until recovery of serum TSH was 9.4 – 6.1 months in TBII-positive and 6.0 – 4.0 months in TBII-negative patients. Recovery of serum TSH at 3, 6, 12, 18, 24, and 30 months, after the normalization of serum T 3 and T 4 were 39%, 62%, 63%, 74%, 88%, and 86% respectively in TBII-positive patients. The corresponding figures in TBII-negative patients were 74%, 91%, 91%, 91%, 94%, and 90% respectively. There was no difference in serum T 3 or T 4 between TBII-positive and TBII-negative patients at 3, 6 and 12 months after normalization of serum T 3 and T 4 , but TSH levels at these time-points were lower in the TBII-positive patients. TBII correlated inversely only with serum TSH.
Conclusions
Continued suppression of serum TSH in patients with Graves- disease during antithyroid drug treatment is related to TBII, pre-treatment severity of hyperthyroidism, and time to normalization of serum T 3 and T 4.
Commentary
Present study confirms and extends previous reports that TBII may be causally related to continuous TSH suppression in treated patients with Graves- hyperthyroidism, despite normal serum T 3 and T 4 concentrations. Evidence supporting a causal relationship is provided by the longer time interval between normalization of serum T 3 / T 4 and normalization of serum TSH in the TBII positive patients, as compared to the TBII-negative patients, and the inverse relation between TBII and TSH, independent of ambient serum T 3 and T 4 concentrations. The mechanism proposed to explain this observation is the binding of TBII to TSH receptors in the pituitary. TSH receptors have been demonstrated in folliculo-stellate cells of the human pituitary. Binding of TSH to these receptors might down-regulate TSH synthesis and release, thereby providing an ultra-short loop feedback in the regulation of TSH. How the folliculo-stellate cells signal to the thyrotroph cells remains to be elucidated. Binding of TBII to the folliculo-stellate TSH receptors might likewise inhibit pituitary TSH release.
The present study also showed that the time period required for normalization of TSH was determined – besides TBII – by pretreatment T 3 levels as well as by the rapidity of normalization of serum T 3 and T 4 . Because pretreatment T 3 was higher in TBII-positive patients, it remains plausible that these two other determinants of TSH recovery time were not independent factors. Nevertheless, the clinical relevance of the present study is that as long as serum TSH is suppressed, dose-adjustments of antithyroid drugs should be guided by serum T 3 and T 3 results and not by serum TSH. Some patients maintain a suppressed TSH for years and, occasionally, one may see patients with clearly decreased FT 4 levels because they receive a dose of antithyroid drugs that is too high in the presence of a TSH that is still suppressed.( Summary and commentary prepared by Wilmar Wiersinga ) Present summary and commentary are related to Chapter N- 11 (Section on Antithyroid Drug Therapy) of TDM
By Emily Lyth on Monday, March 23, 2015 at 11:16 AM
A message from Carrie:
I have noticed quite a few of you only having the TPO antibody test done. This is the incorrect antibody test. The correct antibody tests for Graves’ disease (GD) is TRAb and or TSI.
TRAb is the acronym for Thyroid Receptor Autoantibody, TSH Receptor Antibodies or TSH Receptor AB. TRAb consists of 3 types of antibodies:
- Blocking
- Stimulating
- Neutral
TSI is the acronym for Thyroid Stimulating Immunoglobulins and this is the stimulating part of TRAb. With GD we tend to switch from blocking to stimulating to blocking. But right now I want to talk a bit about TPO.
TPO – Thyroperoxidase AB are antibodies created to mop up peroxidase spills from certain cells. They are markers that there is a problem – but they aren’t the cause of disease.
My TPO’s were 2600+ when first diagnosed and I didn’t have a goiter – Nor did I have Hashimoto’s. The only true test for Hashimoto’s is an ultra sound and or FNA. Extremely high TPO’s should alert your doctor to do more tests to rule out Hashimoto’s, cancer etc.
Peroxidase is an enzyme used during cell metabolism and it should always be safely tucked inside the cell.
Val gives a great explanation:
“If something breaks open that cell examples would be high TSH, TSI, a blow to the neck, cancer, etc. Our immune system will see the peroxidase as something that should not be free and that is why we start to make TPO-antibodies, to clean it out. Sometimes those antibodies can cause more problems to nearby tissues since they bring along other cells that are similar to flame-throwers. If those accidentally rip another cell, well, now you have more loose peroxidase and now more TPOabs are going to be needed.
When a thyroid is being hammered by high TSH or high TSI, theres going to be some inflammation going on too. This is why TPOabs are usually quite high before we start on Antithyroid medications. It’s also why the TPOabs go up higher when we use iodine contrast dyes on CT scans or RAIU scans. Or even when we just eat something with large loads of iodine. Those are all irritating to the thyroid.
But even a blow to the throat can cause TPOabs. Anything that breaks a thyroid cell.”
TPO can destroy the enzyme needed to make T4 and T3.
There are some cells in other body parts that also contain peroxidase. That’s why TPOabs can be seen when you have other issues going on as well ie:
- Hashimotos
- Graves’ disease (up to 95% of patients)
- Primary myxedema
- Thyroid cancer
- Pernicious anemia
- Myasthenia gravis
- Cirrhosis of the liver
- Lupus
- Sjogren’s Syndrome
TPO can even be seen in some healthy people.
By Emily Lyth on Saturday, March 21, 2015 at 12:13 PM
One of our lovely group members was kind enough to share this study that discusses the connection between chronic urticaria (hives) & autoimmune thyroid disease. Links are provided at the bottom of the post–
Some patients with chronic urticaria have autoimmune thyroid disease
(July 2004)
The background of the study. Most patients with chronic urticaria (hives) are not allergic to any identifiable substance, and the urticaria is thought to be an autoimmune disorder. The relationship between chronic urticaria and autoimmune thyroid disease was evaluated in this study.
How the study was done. There were four study groups. One consisted of 45 patients with chronic urticaria (defined as three or more episodes of urticaria weekly for at least six weeks) seen in a dermatology clinic. The second group consisted of 32 patients with goiter, thyroid nodules, hyperthyroidism, or hypothyroidism who had a high serum concentration of antithyroid antibodies. The third group consisted of 22 patients with similar thyroid disorders, but normal serum concentrations of the antibodies. The fourth group consisted of 30 normal subjects.
The results of the study. The 45 patients with chronic urticaria had three or more episodes of urticaria per week for 3 months to 15 years; they had been treated with an antihistamine or glucocorticoid. All had normal thyroid function, but 12 (27 percent) had a high serum concentration of antithyroid peroxidase or antithyroglobulin antibodies; four were considered to have Hashimoto’s thyroiditis, three had thyroid nodules, and five had no thyroid disorder. Six patients in the two thyroid-disorder groups had a history of urticaria, and four of them had urticaria during the one-year follow-up period. None of the normal subjects had a history of urticaria.
The conclusions of the study. Patients with chronic urticaria are more likely to have high serum concentrations of antithyroid antibodies than normal subjects.
The original article. Verneuil L, Leconte C, Ballet JJ, Coffin C, Laroche D, Izard JP, Reznik Y, Leroy D. Association between chronic urticaria and thyroid autoimmunity: a prospective study involving 99 patients. Dermatology 2004;208:98-103.
CRISTIN PHILLIPS FLANDERS·SATURDAY, FEBRUARY 21, 2015·
Iodine-Rich Foods
Baked Potatoes with Skin Serving Size (1 medium potato), 60 micrograms of iodine (40% DV),
MilkServing Size (1 cup), 56 micrograms of iodine (37% DV)
Dried SeaweedServing Size (1/4 ounce), 4,500 micrograms of iodine (3000% DV)
CodServing Size (3 ounces), 99 micrograms of iodine (66% DV)
Fortified Iodized SaltServing Size (1 gram), 77 micrograms of iodine (51% DV)
ShrimpServing Size (3 ounces), 35 micrograms of iodine (23% DV)
Himalayan Crystal SaltServing Size (1/2 gram), 250 micrograms of iodine (167% DV)
Baked Turkey BreastServing Size (3 ounces), 34 micrograms of iodine (23% DV)
Dried PrunesServing Size (5 prunes), 13 micrograms of iodine (9% DV)
Navy BeansServing Size (1/2 cup), 32 micrograms of iodine (21% DV)
Fish SticksServing Size (2 fish sticks), 35 micrograms of iodine (23% DV)
Canned TunaServing Size (3 ounces), 17 micrograms of iodine (11% DV)
Boiled Eggs Serving Size (1 large egg), 12 micrograms of iodine (9% DV)
Plain Yoghurt Serving Size (1 cup), 154 micrograms of iodine (58% DV)
Bananas Serving Size (1 medium banana), 3 micrograms of iodine (2% DV)
StrawberriesServing Size (1 cup), 13 micrograms of iodine (9% DV)
Canned CornServing Size (1/2 cup), 14 micrograms of iodine (9% DV)
LobsterServing Size (100 grams), 100 micrograms of iodine (67% DV)
Cheddar CheeseServing Size (1 ounce), 12 micrograms of iodine (8% DV)
CranberriesServing Size (4 ounces), 400 micrograms of iodine (267% DV)
White BreadServing Size (2 slices), 45 micrograms of iodine (30% DV)
Green BeansServing Size (1/2 cup), 3 micrograms of iodine (2% DV)
Blueberries and Raspberries –mcg of Iodine (0%DV)
Thanks to Jennifer Altintutar
By Cristin Phillips Flanders on Tuesday, February 3, 2015 at 8:09 PM
Pure Encapsulations
Seeking Health
Klaire Labs
NOW Foods
Thorne
Vital Nutrients
Green Pastures (Fermented cod liver oil)
All of the above are generally allergen-free. Check individual manufacturers to verify. (This information can usually be found under “Supplement Facts.”)
By Emily Lyth on Monday, February 2, 2015 at 11:24 AM
Please read this study posted by Val Collins of Graves’ Disease – Research News on high doses of Methimazole:
Endocr Res. 2015;40(1):25-8. doi: 10.3109/07435800.2014.914038. Epub 2014 May 15.
Remission of Graves’ disease is not related to early restoration of euthyroidism with high-dose methimazole therapy.
Kruljac I1, Solter D, Vrkljan AM, Solter M.
Author information
Abstract
Abstract Introduction and aims: The most recent hypothesis postulated that early restoration of euthyroid state in patients with Graves’ disease changes the course of the disease and leads to better disease control. Therefore, we analyzed the efficacy of methimazole therapy and the course of disease in patients with restored euthyroidism and in patients with active disease on first control visit.
PATIENTS AND METHODS:We included 63 patients with total T4 level >190 nmol/L or T3 >7 nmol/L and diffuse goiter with no previous episodes of hyperthyroidism. All patients received initially high doses of methimazole (60-80 mg) followed by a rapid dose reduction.
RESULTS:
Ten percent of patients were excluded from the study due to side effects. Two different groups emerged after 5 weeks of treatment with same dose of methimazole: group 1 with active disease (48%) and group 2 with restored euthyroidism. Further controls on 12th, 24th and 68th weeks of treatment showed no difference in remission rates, number of iatrogenic hypothyroid episodes, and number of exacerbations between the two groups, regardless of methimazole dose. There was no association between age, gender, thyroid hormone levels, and remission and exacerbation rates.
CONCLUSIONS:
Initially, higher methimazole doses with rapid progressive decrease to maintenance dose result in similar remission rates and are followed by similar incidence of adverse side-effect as fixed low dose therapy. Our results indicate that neither an early restoration of euthyroidism nor the difference in methimazole doses influence the course of Graves’ disease.
By Emily Lyth on Saturday, January 3, 2015 at 1:40 PM
As Kathryn shared earlier this morning:
This is a must read for everyone!!!
Our lovely Vikki may be taking a break from the group but she has not taken a break from her research.
She read about research being done on a treatment/cure for autoimmune disease. When she came across some exciting research being done, she actually found contact info and has been corresponding back and forth with one of the scientists himself!!! Can you say tenacity at it’s finest?!?!
Here’s a little blurb on the research:
Scientists discover how to ‘switch off’ autoimmune diseases
Date: September 3, 2014
Source:University of Bristol
Summary: Scientists have made an important breakthrough in the fight against debilitating autoimmune diseases such as multiple sclerosis by revealing how to stop cells attacking healthy body tissue. Rather than the body’s immune system destroying its own tissue by mistake, researchers have discovered how cells convert from being aggressive to actually protecting against disease.
http://www.sciencedaily.com/releases/2014/…/140903092157.htm
Please read the info in that link before reading on.
She received this email from The Scientist (name removed for his privacy):
http://www.sciencedaily.com/releases/2014/…/140903092157.htm
Dear Mrs. Cooley,
We have now completed 2 clinical trials of peptide therapy in multiple sclerosis and have a trial that we hope to start in Graves’ disease in 2015. So, we have designed and produced the peptides for treatment of Graves’ disease and will begin trials as soon as possible.
Vikki asked: Also, is antigen-specific immunotherapy something that any doctor can do here in the United States? Is it even being done? Can it be done?”
David responded: Antigen-specific immunotherapy has been used to treat allergy for over a century. However, the treatment can be dangerous when done with whole allergen. This is why we developed the idea of using peptides because they should work without the danger.
Let’s hope our first trial in patients is successful and we can accelerate this through to being available to you. As with any new treatment, however, there is a great deal of regulation designed to make sure that patients don’t suffer unnecessary side effects. Each new drug has to go through 3 levels of clinical trials.
best wishes,
The Scientist
It’s been a while since she emailed him so she emailed again requesting an update.
Here is his reply:
Dear Vikki,
You can learn more about our activities through the website of the company I founded 12 years ago that is developing the new treatments for autoimmune diseases.www.apitope.com
There is a movie in http://apitope.com/technology/
Please feel free to forward this information to anyone who might be interested.
best wishes,
The Scientist
THIS, dear friends, is why we’re keeping our thyroid!!!
Is this not just fantabulous, happy dance, exciting?!?!!
By Emily Lyth on Thursday, December 18, 2014 at 10:46 PM
Kathryn found a study conducted by the National Institute of Health that confirms the long-term use of Methimazole to treat hyperthyroidism is safe. The study & more information can be found at: http://www.ncbi.nlm.nih.gov/m/pubmed/15879354/
By Emily Lyth on Wednesday, December 10, 2014 at 9:39 PM
A helpful article that explores what thyroid disease is & how you can heal it:
By Emily Lyth on Friday, December 5, 2014 at 3:12 PM
Hi. My name is Graves, and I’m an invisible autoimmune chronic disease that attacks your thyroid gland.
I am now velcroed to you for life.
Others around you can’t see me or hear me, but YOUR body feels me.
I can attack you anywhere and anyhow I please.
I can cause severe pain or, if I’m in a good mood, I can just cause you to ache all over.
Remember when you and energy ran around together and had fun?
I took energy from you, and gave you exhaustion. Try to have fun now!
I can take good sleep from you and in its place, give you brain fog and lack of concentration.
I can make you want to sleep 24/7, and I can also cause insomnia.
I can make you tremble internally or make you feel cold or hot when everyone else feels normal.
I can also give you swollen hands and feet, swollen face and eyelids, swollen everything!
Oh, yeah, I can make you feel very anxious or very depressed, too.
I can also cause other mental health problems.
I can make your hair fall out, become dry and brittle, cause acne, cause dry skin, the sky is the limit with me!
I can make you gain weight and no matter what you eat or how much you exercise, I can keep that weight on you. I can also make you lose weight. I don’t discriminate.
Some of my other autoimmune disease friends often join me, giving you even more to deal with.
If you have something planned, or are looking forward to a great day, I can take that away from you.
You didn’t ask for me. I chose you for various reasons: That virus or viruses you had that you never really recovered from, or that car accident, or maybe it was the years of abuse and trauma (I thrive on stress.) Maybe you have a family history of me. Whatever the cause, I’m here to stay.
I hear you’re going to see a doctor to try and get rid of me. That makes me laugh! Just try.
You will have to go to many, many doctors until you find one who can help you effectively.
You will be put on the wrong thyroid meds for you, pain pills, sleeping pills, energy pills, told you are suffering from anxiety or depression, given anti-anxiety pills and antidepressants.
There are so many other ways I can make you sick and miserable, the list is endless – that high cholesterol, gall bladder issue, blood pressure issue, blood sugar issue, heart issue among others? That’s probably me.
Can’t get pregnant, or have had a miscarriage?
That’s probably me too.
Teeth and gum problems? TMJ? I told you the list was endless.
You may be given a TENs unit, get massaged, told if you just sleep and exercise properly I will go away.
You’ll be told to think positively, you’ll be poked, prodded, and MOST OF ALL, not taken seriously when you try to explain to the doctor how debilitating I am and how sick you really feel.
In all probability you will get a referral from the ‘understanding’ (clueless) doctor, to see a psychiatrist.
Your family, friends and co-workers will all listen to you until they just get tired of hearing about how I make you feel, and just how debilitating I can be.
Some of them will say things like “Oh, you are just having a bad day” or “Well, remember, you can’t do the things you use to do 20 YEARS ago”, not hearing that you said 20 DAYS ago.
Some will start talking behind your back, they’ll call you a hypochondriac, while you slowly feel that you are losing your dignity trying to make them understand, especially when you are in the middle of a conversation with a “normal” person, and can’t remember what you were going to say next. You’ll be told things like, “Oh, my grandmother had that, and she’s fine on her thyroid pill” when you desperately want to explain that I don’t impose myself upon everyone in the exact same way, and just because that grandmother is fine on the medication SHE’S taking, doesn’t mean it will work for you.
I’ve been trying to keep this next part quiet, but since you’re reading this you already know.
The only place you will get the kind of support and understanding in dealing with me, is with other people that have me. They are really the only ones who can truly understand.
I am Graves Disease.
By Emily Lyth on Tuesday, December 2, 2014 at 10:52 AM
Many endocrinologists and doctors are quick to push patients with Graves’ into having RAI, but very few discuss all the dangers involved in choosing this treatment method. Below is a list of links containing information that I have found incredibly helpful and eye-opening. They discuss some of the very real & lesser-known risks involved in RAI treatment. If you are considering RAI as a treatment option, this information is definitely worth exploring before you make such a permanent decision!
1) http://www.stopthethyroidmadness.com/top-reasons-not-to-have-rai/
2) http://www.stopthethyroidmadness.com/rai/
3) http://tampub.uta.fi/bitstream/handle/10024/67755/978-951-44-7081-3.pdf?sequence=1
4) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116221/
5) http://thyroid.about.com/b/2009/10/14/radioactive-iodine-thyroid-eye-ophthalmopathy.htm
By Emily Lyth on Monday, December 1, 2014 at 4:14 PM
Dear Husband of Graves’, This letter is to all of us who are or were married to someone with Graves’ disease. It is a letter from my heart as I know of no other way to talk about it. If in some way it speaks to those of you who are now struggling or have struggled with the loneliness, the frustration at the lack of answers, the inability to help the ones you love, having to make major decisions without your partner, or going through the pain of divorce because of a disease very few understand and fewer still can relate to, then it will have been worth exhuming painful memories that time was mercifully putting to rest.
I’ve heard that the divorce rate skyrockets when someone has Graves’ disease. I am not surprised. This disease works to challenge every reason you had for being married and forces you insidiously to get to the bottom line – that a marriage exists only because you are willing to remain committed to your partner, regardless of anything else.
In a lot of ways my wife and I were fortunate; she was diagnosed with Graves’ disease after approximately nine months, at least that is the closest she and I can pin point when she began to first experience the symptoms we now associate with Graves’. During that time, however, while I always knew my wife loved me, frequently who I was married to was not my wife.
One aspect was the mood swings, the unexpected outbursts of anger and accusation, the unexplainable crying. This took the most work for me to deal with emotionally. I know I unintentionally do or say things that irritate her from time to time. But when compared with how we usually handled these issues, the anger of crying was out of proportion to the crime and it came with no warning. Unfortunately, I found myself putting up a wall between us for protection and I hated the estrangement. I became increasingly on guard when with her. I didn’t want to be hurt. We’ve been married many years and she knew me well enough to know how to get in deep with her accusations. I detested the alienation but felt caught in a “Catch 22”– be on guard to mitigate the hurt and loose the closeness in the relationship. Remain open and get hurt. Fortunately the outbursts happened and then quickly dissipated but only recently has “being on guard” begun to melt.
Another was the feelings of impotence; being powerless to change the circumstances regardless of what you did. I’ve always thought my wife was beautiful and while she is attractive physically, her beauty to me has always had little to do with her looks. I enjoy the way she thinks and what she thinks about. When we talk, I learn something. I enjoy watching her meet people. I love hearing her laugh and am frequently in amazement at her ability to laugh regardless of the circumstances. Together we’ve been through some amazing challenges in life. Her indomitable spirit is what got us through them. While she was going through the worst of the disease, Graves’ took all of that away. All I could do was stand by and watch. Nothing I did changed anything.
She had constant headaches from morning to night and over-the-counter medications didn’t help. She hurt every time she blinked her eyes. Her feet were frequently so swollen they wouldn’t fit in her shoes. The puffiness around her eyes and “bug-eyed” appearance was uncomfortable for others to see. My chest ached as I watched people who previously were attracted by her vivacious personality now avoid her altogether or talked with her in a stilted fashion. I watched her withdraw. I was watching the love of my life shrivel and die while being imprisoned in the role of bystander. All I could do was hold her and cry with her when the unrelenting discomfort got to be too much.
Three and one-half years have now gone by and the nightmare has finally come to a close. The disease went through its cycle and stabilized. My wife has now had corrective surgery to repair much of the physical damage of the disease. She still sleeps with a strip of plastic wrap over her eyes to keep them from drying out during the night and her feet are still swollen although less so. Mostly she has returned to living with that special brand of vitality which I so love. She is laughing again.
Where do you turn when your whole world is turned upside down? How do you cope with a situation of changing emotions, many questions, few answers and no idea when it will all end, if ever? While I survived Graves’ disease, I don’t think I took particularly good care of myself emotionally during this time. I mostly did my “guy thing”; I didn’t talk about it to anyone. It didn’t seem appropriate to talk to my wife, my usual confidante. She already had a full plate without my “stuff”. What about talking to other men? Mostly I didn’t. Occasionally I would talk about the topic when I was desperate and someone asked. But mostly, while I found some willing listeners among my friends, those times were never particularly satisfying. They would sympathize but had little or no experience with which to relate. This whole issue of “where does the husband of Graves’ go for help” is one area I now know I would do differently. I would take the time to find other men in the same predicament and I would talk to them. If nothing else, I would know I was not alone.
Sincerely,
David Bos
Jeffersonville, Indiana
Editor’s Note: David is the husband of Bonnie Bos, Indiana and Kentucky State Director.
Thyroid Hormone and The Female Reproductive System
The functions of the thyroid gland have much to do with a woman’s reproductive system, particularly if the thyroid is overactive or underactive. This imbalance in hormone levels may have the following effects on a woman’s body:
|
Puberty and menstruation |
Thyroid disorders can cause puberty and menstruation to occur abnormally early or late. In addition, abnormally high or low levels of thyroid hormone can cause very light or very heavy menstrual periods, very irregular menstrual periods, or absent menstrual periods (a condition called amenorrhea). |
|
Reproduction |
An overactive or underactive thyroid may also affect ovulation. This is the release of an egg for fertilization. Thyroid disorders may prevent ovulation from occurring at all. In addition, the ovaries are at an increased risk for cyst development if the woman has an underactive thyroid (hypothyroid). Severe hypothyroidism can actually cause milk production in the breast, while preventing ovulation. |
|
Pregnancy and postpartum |
Thyroid disorders during pregnancy can harm the fetus and may lead to thyroid problems in the mother after birth, such as postpartum thyroiditis. A deficiency of thyroid hormone can cause miscarriages, preterm delivery, stillbirth, and postpartum hemorrhage. Women with overactive thyroid during pregnancy are at risk of having more severe morning sickness. Ways of treating overactive thyroid gland during pregnancy must be individually considered. |
|
Menopause |
Thyroid disorders may cause the early onset of menopause (before age 40 or in the early 40s). Some symptoms of overactive thyroid (hyperthyroidism) may also be mistaken for early menopause. These include lack of menstruation, hot flashes, inability to sleep (insomnia), and mood swings. Treating hyperthyroidism can sometimes ease symptoms of early menopause or prevent early menopause from happening. |
*Source – Johns Hopkins Medicine