Is Thyroid Cure Permanently

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Is Thyroid Cure Permanently
Can hyperthyroidism be cured? – Yes, there is a permanent treatment for hyperthyroidism. Removing your thyroid through surgery or destroying your thyroid through medication will cure hyperthyroidism. However, once your thyroid is removed or destroyed, you’ll need to take thyroid hormone replacement medications for the rest of your life.

Can thyroid go back to normal?

Causes of Hyperthyroidism – Hyperthyroidism can be caused by a number of things:

Toxic nodule – A single nodule or lump in the thyroid can produce more thyroid hormone than the body needs and lead to hyperthyroidism. Toxic multinodular goiter – If the thyroid gland has several nodules, those nodules can sometimes produce too much thyroid hormone causing hyperthyroidism. This is most often found in patients over 50 years old. In many cases, a person may have had a multinodular goiter for several years before it starts to produce excess amounts of thyroid hormone. Graves’ disease – Graves’ disease is an autoimmune disorder in which the body’s immune system attacks the thyroid. Patients with Graves’ disease often have enlargement of the thyroid gland and become hyperthyroid. In some patients, the eyes may be affected. Patients may notice the eyes become more prominent, the eyelids do not close properly, a gritty sensation and general irritation of the eyes, increased tear production, or double vision. Like other autoimmune diseases, this condition may occur in other family members and is much more common in women than in men. Sub-acute thyroiditis – This type of hyperthyroidism can follow a viral infection which causes inflammation of the thyroid gland. This inflammation causes the thyroid to release excess amounts of thyroid hormone into the blood stream which leads to hyperthyroidism. Over time the thyroid usually returns to its normal state. Because the stored thyroid hormone has been released, patients may become hypothyroid (where their thyroid gland produces too little thyroid hormone) for a period of time until the thyroid gland can build up new stores of thyroid hormone. Postpartum thyroiditis – Some women develop mild to moderate hyperthyroidism within several months of giving birth, which usually lasts 1 to 2 months. This is often followed by several months of hypothyroidism. Most women recover and have normal thyroid function. Excessive Iodine ingestion – Some food sources with high concentrations of iodine, such as over the counter supplements, kelp tablets, some expectorants, amiodarone (a medication used to treat certain heart rhythm problems) and x-ray dyes, may occasionally cause hyperthyroidism in some patients. In most cases, the hyperthyroidism usually resolves when the supplement is discontinued. Overmedication with thyroid hormone – Patients who take too much thyroid hormone replacement can also develop hyperthyroidism. Patients should have their thyroid hormone levels evaluated by a physician at least once each year and should NEVER give themselves “extra” doses unless directed by a physician. Changes in thyroid medication should always be guided by thyroid function testing.

How long thyroid patients live?

We investigated the association of thyroid function with life expectancy with and without NCD among euthyroid individuals. We found that individuals with low–normal thyroid function live up to 3.7 years longer overall, of which up to 1.9 years longer with NCD, than individuals with high–normal thyroid function.

At what age do thyroid problems start?

An overactive thyroid, also known as hyperthyroidism or thyrotoxicosis, is where the thyroid gland produces too much of the thyroid hormones. The thyroid is a small butterfly-shaped gland in the neck, just in front of the windpipe (trachea). It produces hormones that affect things such as your heart rate and body temperature.

How can I recover my thyroid permanently?

Around 15 million Americans have hypothyroidism (underactive thyroid). However, up to 60% of those with a thyroid disorder are completely unaware of it. Hypothyroidism symptoms include weight gain, memory loss, high blood pressure, and heart disease. Many doctors insist hypothyroidism is incurable and that patients must manage the condition for their entire lives with medications like levothyroxine,

  • Is there a cure for hypothyroidism ? Yes, there is a cure for a majority of cases of hypothyroidism caused by Hashimoto’s.
  • Patients may completely reverse hypothyroidism with an individualized treatment plan including dietary changes, supplements, stress relief, peptide therapy, and thyroid medications.

The board-certified physicians and providers at PrimeHealth have worked with patients to learn how to cure hypothyroidism permanently — and naturally! When patients seek our help, we tailor an individual treatment plan that is both undisruptive to your body’s natural processes and unique to your individual needs.

Can thyroid symptoms go away?

Can hypothyroidism go away on its own? – In some mild cases, you may not have symptoms of hypothyroidism or the symptoms may fade over time. In other cases, the symptoms of hypothyroidism will go away shortly after you start treatment. For those with particularly low levels of thyroid hormones, hypothyroidism is a life-long condition that will need to be managed with medication on a regular schedule.

Does thyroid get worse with age?

Hypothyroidism in Older Adults Hypothyroidism is more common among elderly individuals due to the increasing incidence and prevalence of autoimmune thyroiditis that occurs with aging. Accurate diagnosis of this condition in the elderly may be challenging due to a number of factors including a relative paucity of referable symptoms, confounding findings that may be related to comorbid disorders, changes in thyroid hormone levels that may be related to nonthyroidal illness, and upward shifts in TSH levels that may occur with normal aging.

  • Effective treatment of hypothyroidism in the elderly relies on consideration of potential drug interactions and changes in the metabolic clearance of thyroid hormone that occur with aging.
  • Specific attention should be paid to minimizing the risks of atrial arrhythmias and progressive bone loss that may be associated with iatrogenic thyrotoxicosis caused by over-treatment with excessive doses of levothyroxine.

Mild hypothyroidism identified in the elderly does not appear to be associated with any changes in cognitive function or functional status. Studies that have sought to determine the risk of cardiovascular disease associated with mild hypothyroidism and the potential benefits of treatment targeted to normalize thyroid hormone levels in elderly individuals with mild hypothyroidism have reported conflicting results.

  1. Elderly patients presenting with untreated or undertreated severe hypothyroidism may be particularly susceptible to decompensation that may progress to a state of myxedema coma.
  2. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text,,
  3. Hypothyroidism increases in prevalence and incidence among the elderly.

It is important for clinicians to appreciate certain aspects of hypothyroidism in older individuals. Its clinical manifestations may be less obvious in the setting of somatic complaints and other conditions related to aging. Thyroid function test interpretation may be altered due to the presence of nonthyroidal illness. 4.”> Percentage of Population with High Serum TSH Level (>4.5mU/L). Adapted from Hollowel et al. (). *Excluding persons with reported histories of thyroid disease, goiter, or treatment with thyroid medications. ** Excluding persons with reported histories of thyroid disease, goiter, treatment with thyroid medications, conditions predisposing to thyroid function test abnormalities, or positive antithyroid antibodies () Hypothyroidism is more common in older persons than younger individuals, especially among women, principally due to the rising incidence and prevalence of autoimmune thyroiditis. Furthermore, the incidence of hypothyroidism steadily increases with advancing age (). Estimates of the prevalence of hypothyroidism among the elderly have varied depending on the populations studied and the criteria used to define the condition. An older survey employing the calculated free thyroxine index found that 2.3% of elderly inpatients met criteria for hypothyroidism (). More recent community surveys of populations of healthy adults have found that 7%-14% of elderly subjects have serum thyroid stimulating hormone (TSH) levels above the upper limit of reference ranges (–). Comparable prevalence’s of hypothyroidism have been found in community dwelling and hospitalized older persons. A screening study that evaluated more than 25,000 individuals attending a health fair in Colorado revealed that 10% of men and 16% of women age 65-74 had TSH levels that were increased above the upper limit of the reference range, while 16% of men and 21% of women age 75 and older had increased TSH levels (). The Third National Health and Nutrition Examination Survey (NHANES III) reported that a significantly greater number of women aged 50-59 and 60-69 met criteria for subclinical and clinical hypothyroidism compared to men in the same age ranges. This survey also reported a higher prevalence of increased TSH levels and anti-thyroid antibody titers among whites and Mexican Americans compared to blacks (). A study evaluating geriatric patients under medical care demonstrated that 15% of the women and 17% of the men had previously undiagnosed hypothyroidism (). Similar studies evaluating skilled nursing facility and nursing home residents demonstrated that 7%-12% had evidence of previously undiagnosed hypothyroidism at the time of admission (,). A treatment survey of an unselected population of older adults revealed that 10% of the women and 2% of the men studied were taking a prescribed form of thyroid hormone (). Among this population, 12% of the women and 29% of the men were reportedly taking thyroid hormone preparations for inappropriate reasons. Future estimates of the prevalence of hypothyroidism among the elderly based on current definitions may need to factor in growing evidence that normal TSH distribution curves appear to be shifted towards higher value ranges in older individuals. Age-specific analysis of TSH levels and anti-thyroid antibody titers measured as part of the most recent NHANES study demonstrated that 12% of subjects aged 80 and older without any evidence of underlying autoimmune thyroiditis had TSH levels greater than 4.5 mIU/L (). In this analysis, the upper 95% confidence limit for TSH in euthyroid individuals over age 80 was 7.5 mIU/L (). Dietary iodine content appears to have an impact on the prevalence of hypothyroidism in the elderly. A survey of Chinese adults living in a region of low iodine intake revealed that only 1.0% of elderly subjects studied met criteria for hypothyroidism, while a study of Eastern European nursing home residents revealed that subjects living in regions of abundant iodine intake had six-fold higher rates of hypothyroidism than subjects living in regions of low iodine intake (,). These findings suggest that iodine deficiency may have a protective effect against the development of hypothyroidism in the elderly. Autoimmune thyroiditis is the most common cause of hypothyroidism among the elderly, as it is in younger persons (–). A survey of endocrinology clinic patients revealed that 57% of patients aged 55 and older presenting with primary hypothyroidism carried a diagnosis of autoimmune thyroiditis, while 32% carried a diagnosis of postsurgical hypothyroidism and 12% had a diagnosis of post-radioiodine hypothyroidism (). Only 2% of the patients in this referral population presented with documented evidence of secondary hypothyroidism. The incidence of post-ablative hypothyroidism has been noted to be higher in patients aged 55 and older (). The annual incidence of post-ablative hypothyroidism in this population is estimated to be 8%, with 12% of patients presenting with evidence of thyroid failure in the first year after undergoing treatment with radioactive iodine (,). The incidence of postsurgical hypothyroidism following subtotal thyroidectomy for treatment of hyperthyroidism has been estimated to be 16-27%, with 19% of patients presenting with evidence of thyroid failure in the first year after surgery (). External beam radiation therapy for treatment of head and neck malignancies has been associated with a high incidence of primary hypothyroidism. Up to 28% of patients treated with this modality eventually develop primary hypothyroidism at a median time of 15 months after completion of radiotherapy (). The risk of developing thyroid failure in this setting increases with advancing age. Elderly patients developing hypothyroidism may present with classic symptoms, but complaints are generally even less specific than those reported by younger patients presenting with evidence of thyroid hormone deficiency (–). In part this may be due to patients and physicians ascribing nonspecific complaints to other comorbid disorders common among the elderly, or to the effects of aging itself (). A study that compared the frequency of 24 symptoms of hypothyroidism reported by elderly and nonelderly patients found that complaints of fatigue and weakness were reported by more than 50% of elderly patients, but that significantly fewer complaints were reported by the elderly compared to a nonelderly group (). Elderly patients less often complained of cold intolerance, weight gain, paresthesias, and muscle cramps. Evaluation of a questionnaire administered to patients newly diagnosed with hypothyroidism ascribed to autoimmune thyroiditis showed that while all 13 referable symptoms were more prevalent in subjects younger than 60 years of age, the only referable symptoms that were more prevalent in older subjects were fatigue, dyspnea, and wheezing (). Other neurological symptoms that have been reported to occur more commonly in older patients include hypogeusia and dysgeusia, impaired hearing, and ataxia. Physical findings evident in hypothyroid elderly individuals may include bradycardia, diastolic hypertension, pallor, dry skin, coarse hair, hoarseness, dysarthria, delayed relaxation of deep tendon reflexes, and mental status changes (). The severity of specific findings may be exacerbated by comorbid cardiovascular, neuropsychiatric, dermatologic, or rheumatologic conditions that are more common among the elderly (). In some cases it may be necessary to evaluate responses to thyroid hormone replacement to determine the extent to which certain findings represent manifestations of thyroid hormone deficiency. Morphologic changes in the size and appearance of the thyroid do not appear to increase with aging (). Elderly patients with autoimmune thyroiditis are more likely to present with the atrophic form of the disorder without goiter (). Neuropsychological testing of elderly patients with hypothyroidism has demonstrated that they score lower on Mini-Mental Status Tests and on 5 of 14 specific indices of visual-spatial function, memory, word fluency, attention, and psychomotor function (). Analysis of laboratory test results has demonstrated that 54% of patients diagnosed with hypothyroidism have increased serum creatinine levels that may be correlated with advancing age (). Pericardial effusion is one of the few radiographic findings associated with hypothyroidism, but the true incidence of this complication appears to be lower than previously estimated (). Severe medical complications of hypothyroidism are more common in affected elderly persons. The majority of patients presenting with myxedema coma are elderly. Elderly patients with unrecognized hypothyroidism may be at greater risk for the development of perioperative and intraoperative complications. One study that compared patients with unrecognized hypothyroidism with controls matched for age, sex, and operative procedure identified higher rates of intraoperative hypotension, heart failure, and postoperative gastrointestinal and neuropsychiatric complications in hypothyroid patients (). A prospective study that screened hospitalized patients aged 60 and older for thyroid dysfunction reported that unrecognized overt hypothyroidism in this population may be associated with significantly higher mortality (). Accurate diagnosis of primary hypothyroidism in the elderly relies primarily, as it does in all patients, on the measurement of a sensitive serum TSH level. Although data from the NHANES III study has established that median TSH levels appear to increase with advancing age, the normal upper limit of an established reference range may still be used as a cutoff to confirm the diagnosis of primary hypothyroidism in most elderly patients. While a blood spot TSH level has been shown to be an adequate screening test for the detection of overt primary hypothyroidism in the elderly, it may not be sensitive enough to detect cases of subclinical hypothyroidism characterized by elevated serum TSH levels with normal T4 or free T4 levels (). One study has determined that there may be a negative correlation between age and the degree to which TSH levels are elevated in elderly patients presenting with primary hypothyroidism (). In cases of suspected secondary hypothyroidism that may result from disruption of the anatomy or function of the hypothalamic-pituitary axis, the TSH level may not be relied upon as an accurate index of thyroid function. In this setting the free T4 level may serve as more reliable measure of thyroid hormone production. The interpretation of thyroid function test profiles in hospitalized or institutionalized patients must be tempered by an understanding of how nonthyroidal illnesses may produce changes in TSH and thyroid hormone levels (). The direction and extent of changes observed may depend on the severity of an underlying illness and the point in the course of recovery at which thyroid function tests are measured (). Longitudinal studies have demonstrated that early on in the course of severe illnesses or protracted procedures, TSH levels in euthyroid patients may decline to levels that fall below the lower limits of normal reference ranges (). This change may be paralleled by a decline in T4 and T3 levels that may be particularly pronounced in elderly patients. One study demonstrated that 59% of elderly patients known to be euthyroid had documented low T3 levels measured during a course of hospitalization, whereas another demonstrated that changes in T3 levels detected in elderly hospitalized patients were more closely correlated with the severity of each underlying illness than with advanced age itself (,). Studies have demonstrated a correlation between declining T4 levels and increasing mortality rates in critical care patients (). Free T4 levels measured by equilibrium dialysis or ultrafiltration methods, if they are within reference ranges, may help to distinguish hypothyroidism from the effects of altered thyroid hormone binding that may occur in critically ill patients (). Current data indicates that the normal or low TSH levels found in the presence of low T4 and T3 levels in the setting of nonthyroidal illness likely reflect the combined effects of central hypothyroidism and reduced peripheral generation of T3, effectively representing a deficiency of thyroid hormone. Whether this condition should be treated with administration of thyroid hormone preparations remains controversial. Some observers argue in favor of thyroid hormone replacement, while others weigh against it, without conclusive data to support either viewpoint (,). If a patient survives to recover from nonthyroidal illness, TSH levels may transiently rise above the upper limits of reference ranges (). If thyroid function tests are checked when a transiently increased TSH level precedes increases in low T4 and/or T3 levels, the profile that emerges may appear to be consistent with primary hypothyroidism (). This could lead to unnecessary treatment with thyroid hormone, which would probably be inconsequential. In cases where changes in TSH and thyroid hormone levels may be plausibly ascribed to nonthyroidal illness, the patient’s thyroid function tests should be reassessed one to two weeks later to see if observed changes are resolving. One study that tracked thyroid function test profiles in hospitalized elderly female patients showed that while 14% of the subjects had increased TSH levels and decreased T4 and T3 levels on initial assessment, only 2% were proven to have evidence of underlying primary hypothyroidism during follow up (). Measurement of anti-thyroid antibody levels may help to confirm a suspected diagnosis of autoimmune thyroiditis as the underlying cause of primary hypothyroidism. However, the presence or absence of elevated anti-thyroid antibodies may not be an absolute indicator of the likelihood of eventual development of primary hypothyroidism in elderly individuals. One study that measured TSH and anti-microsomal antibody levels in healthy elderly adults showed that positive titers were detected in only 67% of subjects with TSH levels > 10.0 mIU/L and 18% of subjects with normal TSH levels (). A similar study that measured anti-thyroid antibody levels in nursing home residents detected positive titers in only 64% of the women and 32% of the men presenting with increased TSH levels (). Comparative measurements of anti-thyroglobulin, anti-microsomal, and anti-thyroid peroxidase antibodies have demonstrated that while there may be a similar prevalence of positive anti-microsomal and anti-thyroid peroxidase titers among elderly adults, mean values of anti-thyroid peroxidase antibody levels tend to be much more commonly elevated in this population (). Nonetheless anti-thyroid antibody measurements in the elderly may help to predict the likelihood of progression from subclinical to overt hypothyroidism (). Abnormalities in other routine laboratory test parameters may suggest possible undetected hypothyroidism. Hyponatremia caused by decreased free water excretion may complicate moderate and severe cases of primary hypothyroidism (). Hyperlipidemia characterized by hypercholesterolemia is commonly evident (). Cases of primary hypothyroidism that are severe enough to precipitate myopathy may present with increased creatine phosphokinase levels (). A hypochromic microcytic anemia that is not associated with any detectable hemoglobinopathy or iron deficiency state may be evident in up to 15% of cases of moderate primary hypothyroidism (). Homocysteine and lipoprotein (a) levels may be increased in patients with primary hypothyroidism, potentially contributing to an increased risk of atherosclerotic disease (). Initial treatment of hypothyroidism in elderly patients should typically start with sodium levothyroxine (thyroxine) administered in lower doses than those usually prescribed for healthy younger patients (e.g.0.25 to 0.5 mcg/kg/day). Once cardiovascular tolerance of a starting dose has been assessed, most experts recommend gradually increasing daily doses by 12.5-25 mcg every four to six weeks until adequate replacement is confirmed by repeat TSH measurement. The degree to which this general strategy has been adopted in practice was confirmed by a recent survey of members of the American Thyroid Association (). A recent trial demonstrated that older patients without any underlying cardiovascular disease could be safely started on full replacement doses of thyroxine (1.6 mcg/kg) without any adverse effects (). While a great deal of interest has arisen regarding the potential benefits of adding doses of liothyronine (T3) to thyroxine to approximate physiologic thyroid hormone secretion, a number of randomized trials have shown that this mode of treatment does not have any significant impact on identified symptoms, mood, cognitive function, or quality of life (–). Serial measurements of TSH levels four to six weeks after each change in thyroxine dosage should be used to monitor thyroid hormone replacement therapy. In a comparison trial based on a reference standard of measured TSH response to TRH administration, basal TSH levels proved to be more sensitive to fine alterations in thyroxine doses than basal free T4 or free T3 levels. Most experts recommend targeting a normal TSH range in elderly patients (). While 39% of ATA members recommended targeting a TSH range of 0.5-2.0 mIU/L when treating younger patients, a comparable number reported that they were generally more liberal in their approach to elderly patients, targeting TSH ranges of 1.0-4.0 mIU/L. Treatment with thyroxine has been shown to increase cognitive testing performance and reduce oro-cecal transit time from an average of 135 minutes in a hypothyroid state to 75-95 minutes with adequate replacement (,). While thyroid hormone supplementation to a level that completely corrects the hormonal deficiency may be an optimal goal, some patients with ischemic heart disease may not be able to tolerate full replacement doses of thyroxine (,). One study of patients with known coronary artery disease and primary hypothyroidism reported that precipitation of angina symptoms limited titration of thyroxine in two-thirds of cases, while precipitation of hypothyroid symptoms limited titration of antianginal agents in one-third of cases. Even with the addition of propranolol at maximally tolerated doses, 46% of the patients surveyed rated control of their angina and hypothyroid symptoms as fair to poor (). Thyroxine dose requirements in elderly patients may be related to several factors including declining metabolic clearance, progression of underlying thyroid failure, declining body mass, and interactions with other medications prescribed for the treatment of co-morbid conditions (,). On average, elderly patients with primary hypothyroidism receive initial daily doses that are 20 mcg lower and maintenance daily doses that are 40 mcg lower than those prescribed for younger and middle-aged patients (–). One study suggested that lean body mass may be a better predictor of daily replacement doses than age or weight alone (). Another reported that most of the age-dependent differences in thyroxine requirements noted might be attributed to the effects of chronic disease, since substantially lower average daily replacement doses were reported by elderly patients treated for other chronic medical disorders (). A study that tracked changes in elderly patients’ thyroxine requirements over time based on the etiology of their primary hypothyroidism reported that daily replacement doses increased in patients who initially presented with autoimmune thyroiditis or postsurgical hypothyroidism, decreased in patients who initially presented with post-ablative hypothyroidism, and did not change in patients who initially presented with subclinical hypothyroidism or drug-induced hypothyroidism (). In situations where cognitive or functional impairment may make it difficult for patients to comply with daily administration of thyroxine, alternative dosing schedules may be considered. A study that compared daily administration of thyroxine to twice weekly administration of comparable cumulative daily doses in elderly women showed that both regimens produced similar peak and trough free T4, T3, and TSH levels (). Trials of regimens based on once weekly administration of cumulative daily doses of thyroxine have demonstrated similar results without any evidence of precipitation of thyrotoxicosis (). A number of medications used to treat other comorbid conditions in the elderly may interfere with absorption and metabolism of thyroxine (). Ingestion of 2,000 mg of calcium carbonate has been shown to interfere with the peak and total incremental absorption of a concomitantly administered treatment dose of thyroxine (). Ferrous sulfate, sucralfate, aluminum hydroxide, cholestyramine, colestipol, and raloxifene have also been reported to impair absorption of thyroxine (,). In postmenopausal women with primary hypothyroidism, treatment with estrogen replacement therapy may lead to increased thyroxine dose requirements as a consequence of increased production of thyroid binding globulin (TBG) (). Women with hormonally-responsive breast cancer who receive fluoxymesterone may require substantially lower doses of thyroxine during courses of treatment, as exposure to this androgenic steroid may decrease effective TBG production (). Long-term administration of phenytoin, carbamazepine, phenobarbital, or rifampin in the setting of treated primary hypothyroidism typically increases metabolism of thyroxine, increasing the dose of thyroxine required to provide optimal replacement (–). Overtreatment with excessive doses of thyroxine may be associated with significant morbidity in the elderly. Palpitations, anxiety, tremulousness, irritability, insomnia, heat intolerance, hyperdefecation, and weight loss may be precipitated or exacerbated by iatrogenic thyrotoxicosis. In elderly patients, exposure to excessive amounts of thyroid hormone may be associated with increased risks of atrial fibrillation, other tachyarrhythmias, and progressive declines in bone mineral density (). A prospective study of the incidence of atrial arrhythmias in patients aged 60 and older determined that over the course of a 10-year period, the relative risk of development of new-onset atrial fibrillation in subjects with initial TSH levels < 0.1 mIU/L was 3.1 when compared to subjects with normal TSH levels (). Further analysis revealed that suppressed TSH levels identified in 77% of these subjects were attributable to iatrogenic thyrotoxicosis resulting from overtreatment. A study that tracked bone mineral density changes in women treated with thyroxine documented greater mean rates of decline in the lumbar spines of those with suppressed TSH levels (). A recent cohort study that tracked TSH and free T4 and T3 levels in healthy aging adults in tandem with inventories of medication use reported that half of the cases of prevalent and incident thyrotoxicosis identified could be attributed to over-treatment with levothyroxine (). Mild or subclinical hypothyroidism, which is characterized by an increased TSH level with concomitant free thyroid hormone levels that fall within normal limits, is very common among elderly men and women. The estimated prevalence of this condition has varied from 4-15%. A study evaluating a community of healthy elderly adults in the southwest of France reported that 4.2% of subjects presenting with increased TSH levels had normal free T4 levels (). Within this group, mild hypothyroidism was linked with an increased prevalence of symptoms of depression. A study that evaluated thyroid function profiles in a bi-ethnic urban community reported that mild hypothyroidism was more commonly identified in females and non-Hispanic white subjects than Hispanic subjects (). Stratified analysis of the impact of mild hypothyroidism in this population revealed no significant alterations in health status measures in subjects with TSH levels ranging between 4.7-10.0 mIU/L. A study that inventoried clinical findings of hypothyroidism in a population of geriatric clinic patients reported that while 15.4% of the men and 14.6% of the women screened met criteria for mild hypothyroidism, the incidence of symptoms and signs consistent with thyroid hormone deficiency detected in these subjects was similar to that reported for euthyroid subjects (). An array of studies that have tracked changes in thyroid function in cohorts of aging subjects in the United States, Australia, the Netherlands, Spain, the United Kingdom, and China have reported that the development of hypothyroidism in elderly patients does not appear to be associated with any change in cognitive function, increased levels of depression, or diminished ability to perform activities of daily living (–). A study that measured an array of anthropometric, biochemical, and neuropsychiatric parameters in Korean subjects aged 65 years and older showed that subclinical hypothyroidism did not appear to be associated with any discernible metabolic or neuropsychiatric derangements (). A study that evaluated subgroups of subjects enrolled in the Health, Aging, and Body Composition study found that those determined to have mild subclinical hypothyroidism (defined by a TSH level of 4.5-7.0 mIU/L with normal thyroid hormone levels) demonstrated better mobility, cardiorespiratory fitness, and walking ease than subjects who were euthyroid or determined to have moderate subclinical hypothyroidism (defined by a TSH level of 7.0-20.0 with normal thyroid hormone levels) (). An analysis of subgroups in this cohort study identified increased odds of prevalent metabolic syndrome among subjects with TSH levels > 10 (). A study that evaluated postmenopausal women at risk for development of osteoporosis reported that subclinical hypothyroidism was not associated with decreased bone mineral density or an increased risk of vertebral or non-vertebral fracture (). Several longitudinal studies have tracked the natural history of untreated mild hypothyroidism in elderly persons. A study of nursing home residents confirmed that over time TSH levels declined to normal ranges in 51% of subjects with initial TSH levels that were lower than 6.8 mIU/L (). Serial TSH levels were persistently elevated in the remainder of these subjects and in all subjects with initial TSH levels greater than 6.8 mIU/L. A similar study that stratified subjects on the basis of anti-thyroid antibody levels reported that 80% of elderly adults with mild hypothyroidism with initial measured anti-microsomal antibody titers greater than 1:1,600 eventually progressed to develop overt hypothyroidism requiring treatment with thyroxine replacement therapy (). A study that tracked 505 subjects diagnosed with mild hypothyroidism over time showed that positive anti-thyroid peroxidase antibodies and higher total cholesterol levels measured at baseline were associated with increased odds of eventual progression to overt hypothyroidism (). Two studies showed that when elderly patients diagnosed with subclinical hypothyroidism were tracked over a span of 4-4.2 years, 44-54% demonstrated normalization of TSH levels consistent with reversion to a euthyroid state (,). Findings that were associated with reversion included lower baseline TSH levels, homogenous echotexture of thyroid tissue on ultrasound imaging, and an absence of detectable anti-thyroid peroxidase antibodies. Questions have been raised about the possible association of mild hypothyroidism with an increased risk of cardiovascular disease in the elderly. One study that confirmed the presence of mild hypothyroidism in 10.8% of subjects drawn from a cohort of postmenopausal women reported a greater age-adjusted prevalence of coronary and aortic atherosclerosis in mildly hypothyroid women (). Even stronger associations between mild hypothyroidism and atherosclerotic disease were noted among postmenopausal women with elevated anti-thyroid antibody levels. Another study that evaluated the prevalence of peripheral vascular disease among nursing home residents reported that 78% of subjects with mild hypothyroidism presented with reproducible claudication, whereas symptomatic peripheral vascular disease was only identified in 17% of euthyroid subjects (). A study that evaluated thyroid function in patients enrolled in a study of pre-existing heart failure reported that subclinical hypothyroidism presenting with TSH levels ≥ 7 mIU/L was associated with an increased risk of a need for the use of ventricular assist devices, heart transplantation, and death (). Population-based studies that have tracked thyroid function in elderly subjects have reported differing results regarding risks of cardiovascular disease. A study that examined community-dwelling subjects aged 70-79 years enrolled in the Health, Aging, and Body Composition study found that subclinical hypothyroidism was associated with an increased incidence of congestive heart failure (). A study that examined subjects aged 65 years and older enrolled in the Cardiovascular Health study found that subclinical hypothyroidism was not associated with an increased incidence of coronary artery disease, cerebrovascular disease, cardiovascular mortality, or all-cause mortality (). Analysis of subgroup data tracked over the course of 12 years and echocardiographic parameters tracked over the course of 5 years demonstrated that subjects with TSH levels ≥10.0 mIU/L had a higher incidence of heart failure events, a greater increase in left ventricular mass, and appreciable changes in measurements reflecting changes in diastolic function compared to euthyroid subjects (). Two meta-analyses that analyzed data from a range of prospective cohort studies incorporating measurements of thyroid function identified a modest increase in the risk of coronary artery disease and associated mortality in subjects determined to have evidence of subclinical hypothyroidism (,). More recent analyses of subgroups tracked in cohort studies have reported that persistent subclinical hypothyroidism does not appear to be associated with an increased risk of all-cause mortality, cardiovascular mortality, coronary artery disease, myocardial infarction, or congestive heart failure (–). An analysis of NHANES III data has identified increased mortality in subjects diagnosed with concurrent subclinical hypothyroidism and congestive heart failure, and a retrospective cohort study from Israel involving 17,440 patients with subclinical thyroid disease showed that TSH levels > 6.35 mIU/L were associated with increased mortality (,). Consideration of treatment of mild hypothyroidism in the elderly is often predicated on the notion that restoration of normal thyroid hormone levels might help to relieve symptoms that could be exacerbated by a deficiency of thyroid hormone. The Thyroid Hormone Replacement for Untreated Older Adult with Subclinical Hypothyroidism (TRUST) trial was specifically designed to address this question (). It randomized 737 subjects ≥ 65 years of age with persistent subclinical hypothyroidism to double-blinded placebo-controlled administration of doses of thyroxine adjusted to normalize TSH levels. Assessment based on a thyroid-related quality-of-life questionnaire after one year of treatment showed no difference in hypothyroid symptom scores or tiredness scores. An analysis that combined data from 146 TRUST trial subjects ≥ 80 years of age with data from 145 subjects enrolled in the Institute for Evidence-Based Medicine in Old Age 80-plus trial who were evaluated with a similar protocol also showed no improvement in hypothyroid symptoms or fatigue; however, a majority of those with elevated TSH levels had values below 7 mIU/L (). The attendant risks of iatrogenic thyrotoxicosis in elderly individuals must be taken into account when weighing the potential risks and benefits of thyroid hormone replacement (). Partial or complete reversibility of hypercholesterolemia has been shown to accompany thyroxine treatment of mild hypothyroidism in the majority of small interventional trials addressing this issue (). Lowering of lipoprotein (a) levels has been shown in some, but not all studies (). Hyperhomocysteinemia in patients with mild hypothyroidism has not been shown to be reversed with thyroxine therapy. A nested trial incorporated in the TRUST trial showed that normalization of TSH levels with levothyroxine for a span of one year did not have any impact on carotid intima media thickness or carotid atherosclerosis (). Patients with severe hypothyroidism may present in a state of pronounced multisystem failure termed myxedema coma (,). Elderly patients with untreated or undertreated primary hypothyroidism and comorbid disorders may be particularly susceptible to decompensation that leads to onset and progression of this life-threatening condition (,). In addition to coma, there may be hypothermia, bradycardia, hypotension, congestive heart failure, ileus, and hypoventilation with hypercapnia and respiratory acidosis. In situations where historical information may be unobtainable, physical examination may reveal evidence of prior thyroid surgery, laryngeal surgery, or head and neck external beam radiation therapy. Radiographic studies may reveal pericardial effusions, which may also be reflected in low voltage waves on electrocardiograms. Although such pericardial fluid collections may be large, they are usually not hemodynamically significant. Laboratory evaluation confirming severe hypothyroidism may also reveal evidence of hyponatremia, hypoglycemia, and/or adrenal insufficiency. Myxedema coma is an endocrine emergency with a mortality rate that may approach 40% (). In addition to older age, factors that may be associated with an increased risk of mortality include comorbid cardiovascular disease and treatment with high-dose thyroxine replacement therapy (). Generally recommended supportive measures include critical care-level monitoring of vital signs, careful external rewarming with heating blankets, correction of fluid and electrolyte imbalances, avoidance of hypnotics and sedatives, empiric treatment of suspected underlying infections, and mechanical ventilatory support as indicated. Given the theoretical risk of concomitant adrenal insufficiency due to polyglandular autoimmune syndromes or hypothalamic-pituitary compromise, many experts recommend empiric treatment with stress-dose glucocorticoids until definitive stimulatory testing can be performed. Recommendations regarding the dose and composition of thyroid hormone preparations that should be administered to treat myxedema coma differ. Most experts concur that intravenous thyroxine should be used to circumvent impaired gastrointestinal absorption. Some have recommended initial thyroxine loading doses, while others have advocated co-administration of liothyronine (T3). Treatment of critically ill hypothyroid patients with high-dose thyroxine has been associated with a significant increase in cardiac index due to increased heart rate and stroke volume with decreased systemic vascular resistance (). Although the onset of action of liothyronine is more rapid than thyroxine, supraphysiologic T3 levels measured after treatment have been correlated with increased mortality in older patients presenting with myxedema coma (). A judicious approach may involve administration of a loading dose of 200-300 mcg of intravenous thyroxine followed by administration of 50 mcg daily. Depending on the estimated risk of underlying cardiovascular disease, a loading dose of 5-25 mcg of liothyronine may be administered concomitantly followed by doses of 2.5-5 mcg every eight hours until clinical improvement is evident. Intravenous hydrocortisone may be administered in stress doses of 50-100 mg every 8 hours while testing for underlying adrenal insufficiency is performed. Professional organizations and task forces have issued a range of recommendations concerning the advisability and timing of biochemical screening for hypothyroidism in adult populations () (–). Screening Recommendations for Hypothyroidism in Adults

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Guideline Methods used to analyze evidence Organization Year of publication
American Thyroid Association guidelines for the detection of thyroid dysfunction Narrative literature review Expert opinion American Thyroid Association 2000
Consensus statement for good practice and audit measures in the management of hypothyroidism and hyperthyroidism Narrative literature review Expert opinion Royal College of Physicians of London Society for Endocrinology 1996
Laboratory medicine practice guideline for the diagnosis and monitoring of thyroid disease testing Narrative literature review Expert opinion American Association of Clinical Chemists American Association of Clinical Endocrinologists American Thyroid Association Endocrine Society National Academy Clinical Biochemistry 1990, in progress
Periodic health examinations: summary of AAFP policy recommendations & age charts Based on systematic review performed by US Preventive Services Task Force Expert opinion American Academy of Family Physicians 1996, 2001
Screening for thyroid disease Systematic review Meta-analysis of observational trials American College of Physicians – American Society of Internal Medicine 1997
Screening for thyroid disease Systematic review US Preventive Services Task Force 1996
AACE clinical practice guidelines for the evaluation and treatment of hyperthyroidism and hypothyroidism Narrative literature review Expert opinion American Association of Clinical Endocrinologists American College of Endocrinology 1996
Treatment guidelines for patients with hyperthyroidism and hypothyroidism Narrative literature review Expert opinion American Thyroid Association 1995, 1999
Screening for thyroid disorders and thyroid cancer in asymptomatic adults Systematic review Canadian Task Force on Preventive Health Care 1994, 1999

A panel of invited experts representing the American Thyroid Association, the American Association of Clinical Endocrinologists, and the Endocrine Society at a consensus development conference found a paucity of evidence regarding the morbidity and impact of subclinical thyroid disease, as well as the potential complications of instituting therapy.

  1. Consequently, this panel concluded that there was insufficient evidence to support routine population-based screening of asymptomatic adults.
  2. However, the panel did conclude that the weight of available evidence supported the adoption of aggressive case-finding strategies in patients at high risk for the development of hypothyroidism.

Specific groups identified as being at increased risk for thyroid dysfunction include women aged 60 years and older and patients with histories of atrial fibrillation, thyroid surgery, radioactive iodine treatment, external beam radiation therapy, or family members with confirmed thyroid disease.

A guideline issued by the American College of Physicians states that it is reasonable to check TSH levels in women aged 50 years and older presenting with symptoms that may be consistent with thyroid dysfunction, given the high prevalence of undiagnosed thyroid disorders among that population (–). The Policy Recommendations for the Periodic Health Exam published by the American Academy of Family Physicians take a more neutral stance, recommending against routine screening in patients less than 60 years old without any specific provisions ().

The United States Preventive Services Task Force and the Canadian Task Force on the Periodic Health Examination have both concluded that there is not enough evidence regarding the impact of diagnosis and treatment of detectable thyroid disease to rule for or against routine screening of asymptomatic adults (,).

  1. Utility analysis based on decision modeling has demonstrated that routine periodic screening for mild hypothyroidism may become more cost-effective with increasing age ().
  2. Studies focusing on actual screening of identified populations of elderly adults have reported mixed results.
  3. One study reported that selection of candidates based on body mass index, symptoms consistent with thyroid dysfunction, or a family history of thyroid disease failed to identify the majority of elderly patients eventually confirmed to have elevated or suppressed TSH levels ().

Another study that evaluated elderly patients presenting with suspected dementia revealed that hypothyroidism was the second most common undiagnosed disorder contributing to cognitive impairment (). A similar study reported that measurement of TSH levels identified hypothyroidism in 3.6% of elderly adults presenting for evaluation of mental status changes ().

  • Screening studies involving hospitalized patients reported that 2.3% of geriatric inpatients and 11.2% of patients admitted for elective cardiac surgery had thyroid function profiles consistent with hypothyroidism ().
  • These findings are not surprising in light of the substantial prevalence of hypothyroidism among elderly patients in general.

An analysis of profiles of TSH and thyroid hormone levels tracked in subjects enrolled in the Birmingham Elderly Thyroid Study reported high stability of euthyroid and subclinical hypothyroid indices over a 5 year interval, indicating that repeat testing may not be warranted in this population ().1.

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Somwaru LL, Rariy CM, Arnold AM, Cappola AR. The natural history of subclinical hypothyroidism in the elderly: the cardiovascular health study.J. Clin. Endocrinol. Metab.2012; 97 (6):1962–1969.129. Hak AE, Pols HA, Visser TJ, Drexhage HA, Hofman A, Witteman JC.

Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: the Rotterdam Study. Ann. Intern. Med.2000; 132 (4):270–278.130. Mya MM, Aronow WS. Increased prevalence of peripheral arterial disease in older men and women with subclinical hypothyroidism.J.

Gerontol. A Biol. Sci. Med. Sci.2003; 58 (1):68–69.131. Kannan L, Shaw PA, Morley MP, Brandimarto J, Fang JC, Sweitzer NK, Cappola TP, Cappola AR. Thyroid Dysfunction in Heart Failure and Cardiovascular Outcomes. Circ Heart Fail.2018; 11 (12):e005266.132. Rodondi N, Newman AB, Vittinghoff E, de Rekeneire N, Satterfield S, Harris TB, Bauer DC.

Subclinical hypothyroidism and the risk of heart failure, other cardiovascular events, and death. Arch. Intern. Med.2005; 165 (21):2460–2466.133. Cappola AR, Fried LP, Arnold AM, Danese MD, Kuller LH, Burke GL, Tracy RP, Ladenson PW. Thyroid status, cardiovascular risk, and mortality in older adults. JAMA.2006; 295 (9):1033–1041.134.

Rodondi N, Bauer DC, Cappola AR, Cornuz J, Robbins J, Fried LP, Ladenson PW, Vittinghoff E, Gottdiener JS, Newman AB. Subclinical thyroid dysfunction, cardiac function, and the risk of heart failure. The Cardiovascular Health study.J. Am. Coll. Cardiol.2008; 52 (14):1152–1159.135.

Ochs N, Auer R, Bauer DC, Nanchen D, Gussekloo J, Cornuz J, Rodondi N. Meta-analysis: subclinical thyroid dysfunction and the risk for coronary heart disease and mortality. Ann. Intern. Med.2008; 148 (11):832–845.136. Rodondi N, den Elzen WPJ, Bauer DC, Cappola AR, Razvi S, Walsh JP, Asvold BO, Iervasi G, Imaizumi M, Collet T-H, Bremner A, Maisonneuve P, Sgarbi JA, Khaw K-T, Vanderpump MPJ, Newman AB, Cornuz J, Franklyn JA, Westendorp RGJ, Vittinghoff E, Gussekloo J., Thyroid Studies Collaboration.

Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA.2010; 304 (12):1365–1374.137. Waring AC, Harrison S, Samuels MH, Ensrud KE. LeBLanc ES, Hoffman AR, Orwoll E, Fink HA, Barrett-Connor E, Bauer DC, Osteoporotic Fractures in Men (MrOS) Study.

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Rhee CM, Curhan GC, Alexander EK, Bhan I, Brunelli SM. Subclinical hypothyroidism and survival: the effects of heart failure and race.J. Clin. Endocrinol. Metab.2013; 98 (6):2326–2336.141. Grossman A, Weiss A, Koren-Morag N, Shimon I, Beloosesky Y, Meyerovitch J. Subclinical Thyroid Disease and Mortality in the Elderly: A Retrospective Cohort Study.

Am.J. Med.2016; 129 (4):423–430.142. Stott DJ, Rodondi N, Kearney PM, Ford I, Westendorp RGJ, Mooijaart SP, Sattar N, Aubert CE, Aujesky D, Bauer DC, Baumgartner C, Blum MR, Browne JP, Byrne S, Collet T-H, Dekkers OM, den Elzen WPJ, Du Puy RS, Ellis G, Feller M, Floriani C, Hendry K, Hurley C, Jukema JW, Kean S, Kelly M, Krebs D, Langhorne P, McCarthy G, McCarthy V, McConnachie A, McDade M, Messow M, O’Flynn A, O’Riordan D, Poortvliet RKE, Quinn TJ, Russell A, Sinnott C, Smit JWA, Van Dorland HA, Walsh KA, Walsh EK, Watt T, Wilson R, Gussekloo J., TRUST Study Group.

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Does thyroid get worse over time?

Hyperthyroidism is treatable. Some causes may go away without treatment. Hyperthyroidism caused by Graves disease usually gets worse over time. It has many complications, some of which are severe and affect quality of life.

Can I live a normal life without a thyroid?

Life without your thyroid – If your doctor recommends thyroid removal or you’ve already had your thyroid removed, you must partner with your doctor to optimize thyroid hormone replacement. This involves routinely checking your thyroid hormone levels to avoid overtreatment and undertreatment.

The body must have just enough thyroid hormone. Too much or too little causes symptoms. It can take some time to find the optimal dose and stabilize your symptoms. However, thyroid hormone replacement therapy is fairly straightforward. Aside from having your thyroid levels tested regularly and taking medication daily to give your body the thyroid hormone it needs, people without a thyroid live an otherwise normal life.

Adjusting to life without your thyroid means taking medication and checking in with your doctor. Most people adjust easily. The most important aspect is making sure to take your medication each day. If you have your thyroid and have symptoms, Dr. Morayati can perform a comprehensive,

  1. If you need replacement therapy, we can help.
  2. To learn more, and with Dr.
  3. Morayati at our Burlington, North Carolina office to discuss your thyroid health.
  4. Here at Burlington Medical Center, we offer in-person and appointments.
  5. Heart disease is the leading cause of mortality in the United States, and excessive cholesterol is a major risk factor.

Take action now to lower your cholesterol to help keep your heart in the best shape possible. High blood pressure can sneak up on you, silently causing damage without causing obvious symptoms. Getting to know the subtle signs means you can take action sooner to protect your heart health.

  • When you have gestational diabetes, it’s normal to wonder if you’ll have it after pregnancy.
  • It’s important to work closely with your health care provider to manage diabetes to reduce the chances of it recurring.
  • Developing weak bones doesn’t have to be an inevitable part of getting older.
  • There are risk factors that you can control.

Learn what you need to do to help ward off osteoporosis and keep your bones as strong as possible. Symptoms of thyroid disease are often mistaken for other things like stress, or aging. If you notice changes in your health, or don’t feel quite right, it’s always best to seek an evaluation to get to the bottom of things.

How do I know if my thyroid is OK?

Your thyroid is a small, butterfly-shaped gland in your neck, along the front of your windpipe. It makes hormones that help control many parts of your metabolism, like how fast your heart beats and how fast you burn calories. Women are more likely to have a problem with their thyroid than men – about 1 in 8 women are affected.

Larger appetite than usualSudden weight loss, even though you’re eating the same amount of food or moreFast or uneven heartbeat or sudden pounding of your heart ( palpitations )Nervousness, anxiety, or irritabilityTrembling in your hands and fingers (called tremors) Sweating Changes in your periodIncreased sensitivity to heatChanges in bowel movements, especially more frequent onesSwelling at the base of your neckFeeling tired or like your muscles are weak Trouble sleeping Thinner skin Fine, brittle hair

It’s rare, but you also could have thyroid eye disease. It’s a condition that makes your eyes red and swollen to the point that they seem to bulge. This also can cause blurred or double vision, tearing, and discomfort, and can make you more sensitive to light.

Feel cold Get tired more easilyHave dry skin Be constipated Be forgetfulFeel down or depressed Weight gain Increase in cholesterol levelMuscle weakness Thinning hair Hoarseness

A simple blood test to check your thyroid’s hormone levels is all that’s needed to find out if you have hypothyroidism, For hyperthyroidism, your doctor will see if your thyroid gland is bigger than it should be or if your pulse is too fast. They’ll also look for a tremor in your fingers when you hold them out straight.

  1. If they think you may have it, they’ll want to do a blood test to check your thyroid hormone levels.
  2. They may also recommend a thyroid scan using a small amount of radioactive tracer to see how your thyroid is working.
  3. Another option is a test called a radioactive iodine uptake test (RAIU) to see if it’s working like it should.

For this, you’ll take a small dose of radioactive iodine by mouth, A sensor will be used to find out how much of the iodine your thyroid takes in. The tracer will then leave your body when you pee.

What food should be avoided in thyroid?

Foods to Avoid if You Have Hypothyroidism – Limit or try to avoid these six types of food if you have hypothyroidism.

Cruciferous vegetables – Vegetables such as broccoli, cabbage, kale and Brussels sprouts can inhibit the production of thyroid hormone. This is especially common in those who have an iodine deficiency. Digesting these vegetables can block the ability to absorb iodine, which is needed for normal thyroid function. Cooking cruciferous vegetables reduces the adverse effect on the thyroid. It is suggested that a limit of five ounces per day doesn’t seem to have negative effects on thyroid function.

Gluten – Gluten is the protein — found in foods processed in wheat, rye and other grains — that irritate the small intestine and hinder the absorption of thyroid hormone replacement. If you do decide to eat gluten, choose whole-grain varieties of pasta, bread and rice. This helps to reduce bowel irregularity, a common symptom of underactive thyroid. It’s important to remember to take your hypothyroidism medication a few hours before or after eating these high-fiber foods as not to interfere with thyroid hormone absorption.

Fatty foods – Fats are known to upset your body’s ability to absorb thyroid replacement hormones. Fats can also prevent the thyroid’s natural ability to produce hormones. Physicians recommend that you cut out all fried foods and limit your intake of fats from butter, mayonnaise and fatty meats.

Sugary Foods – A side effect of hypothyroidism is a slowed metabolism. This can cause weight gain if limitations are not in place. Physicians state that you’ll want to avoid foods with too much sugar because they don’t offer nutritional value. Try to reduce your sugar intake or completely eliminate sugar from your diet.

Coffee – Caffeine can block absorption of thyroid hormone replacements. Coffee also has the ability to interfere with the natural thyroid hormone T4 that is absorbed through the stomach. Take your medication with water and skip the coffee for at least 30 minutes before and after.

Processed Foods – These types of foods typically contain high levels of sodium. It is suggested that people with hypothyroidism should avoid sodium due to the already higher risk of having high blood pressure. Sodium only increases this risk. When purchasing food, be sure to look at the label and choose items with the lowest amounts of sodium. According to the U.S. Centers of Disease Control and Prevention, those with a higher risk of high blood pressure should limit their sodium intake to 1,500 milligrams daily instead of the recommended 2,300 milligrams.

These six types of food can contribute to difficulties in your thyroid’s natural hormone production and any hormone replacement medication you may take. Limiting or completely avoiding these foods will help with your hypothyroidism and treatment. Looking for a specialist? and find a physician that fits your needs.

Can you live a full life without a thyroid?

Can I Live Without My Thyroid Gland? As part of the endocrine system, the thyroid gland plays a crucial role in your health. Located at the base of your neck, the thyroid gland produces hormones that control a number of functions, including your heart rate and how quickly your body burns calories.

Does thyroid disease get worse with age?

Hypothyroidism in Older Adults Hypothyroidism is more common among elderly individuals due to the increasing incidence and prevalence of autoimmune thyroiditis that occurs with aging. Accurate diagnosis of this condition in the elderly may be challenging due to a number of factors including a relative paucity of referable symptoms, confounding findings that may be related to comorbid disorders, changes in thyroid hormone levels that may be related to nonthyroidal illness, and upward shifts in TSH levels that may occur with normal aging.

  1. Effective treatment of hypothyroidism in the elderly relies on consideration of potential drug interactions and changes in the metabolic clearance of thyroid hormone that occur with aging.
  2. Specific attention should be paid to minimizing the risks of atrial arrhythmias and progressive bone loss that may be associated with iatrogenic thyrotoxicosis caused by over-treatment with excessive doses of levothyroxine.

Mild hypothyroidism identified in the elderly does not appear to be associated with any changes in cognitive function or functional status. Studies that have sought to determine the risk of cardiovascular disease associated with mild hypothyroidism and the potential benefits of treatment targeted to normalize thyroid hormone levels in elderly individuals with mild hypothyroidism have reported conflicting results.

Elderly patients presenting with untreated or undertreated severe hypothyroidism may be particularly susceptible to decompensation that may progress to a state of myxedema coma. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text,, Hypothyroidism increases in prevalence and incidence among the elderly.

It is important for clinicians to appreciate certain aspects of hypothyroidism in older individuals. Its clinical manifestations may be less obvious in the setting of somatic complaints and other conditions related to aging. Thyroid function test interpretation may be altered due to the presence of nonthyroidal illness. 4.”> Percentage of Population with High Serum TSH Level (>4.5mU/L). Adapted from Hollowel et al. (). *Excluding persons with reported histories of thyroid disease, goiter, or treatment with thyroid medications. ** Excluding persons with reported histories of thyroid disease, goiter, treatment with thyroid medications, conditions predisposing to thyroid function test abnormalities, or positive antithyroid antibodies () Hypothyroidism is more common in older persons than younger individuals, especially among women, principally due to the rising incidence and prevalence of autoimmune thyroiditis. Furthermore, the incidence of hypothyroidism steadily increases with advancing age (). Estimates of the prevalence of hypothyroidism among the elderly have varied depending on the populations studied and the criteria used to define the condition. An older survey employing the calculated free thyroxine index found that 2.3% of elderly inpatients met criteria for hypothyroidism (). More recent community surveys of populations of healthy adults have found that 7%-14% of elderly subjects have serum thyroid stimulating hormone (TSH) levels above the upper limit of reference ranges (–). Comparable prevalence’s of hypothyroidism have been found in community dwelling and hospitalized older persons. A screening study that evaluated more than 25,000 individuals attending a health fair in Colorado revealed that 10% of men and 16% of women age 65-74 had TSH levels that were increased above the upper limit of the reference range, while 16% of men and 21% of women age 75 and older had increased TSH levels (). The Third National Health and Nutrition Examination Survey (NHANES III) reported that a significantly greater number of women aged 50-59 and 60-69 met criteria for subclinical and clinical hypothyroidism compared to men in the same age ranges. This survey also reported a higher prevalence of increased TSH levels and anti-thyroid antibody titers among whites and Mexican Americans compared to blacks (). A study evaluating geriatric patients under medical care demonstrated that 15% of the women and 17% of the men had previously undiagnosed hypothyroidism (). Similar studies evaluating skilled nursing facility and nursing home residents demonstrated that 7%-12% had evidence of previously undiagnosed hypothyroidism at the time of admission (,). A treatment survey of an unselected population of older adults revealed that 10% of the women and 2% of the men studied were taking a prescribed form of thyroid hormone (). Among this population, 12% of the women and 29% of the men were reportedly taking thyroid hormone preparations for inappropriate reasons. Future estimates of the prevalence of hypothyroidism among the elderly based on current definitions may need to factor in growing evidence that normal TSH distribution curves appear to be shifted towards higher value ranges in older individuals. Age-specific analysis of TSH levels and anti-thyroid antibody titers measured as part of the most recent NHANES study demonstrated that 12% of subjects aged 80 and older without any evidence of underlying autoimmune thyroiditis had TSH levels greater than 4.5 mIU/L (). In this analysis, the upper 95% confidence limit for TSH in euthyroid individuals over age 80 was 7.5 mIU/L (). Dietary iodine content appears to have an impact on the prevalence of hypothyroidism in the elderly. A survey of Chinese adults living in a region of low iodine intake revealed that only 1.0% of elderly subjects studied met criteria for hypothyroidism, while a study of Eastern European nursing home residents revealed that subjects living in regions of abundant iodine intake had six-fold higher rates of hypothyroidism than subjects living in regions of low iodine intake (,). These findings suggest that iodine deficiency may have a protective effect against the development of hypothyroidism in the elderly. Autoimmune thyroiditis is the most common cause of hypothyroidism among the elderly, as it is in younger persons (–). A survey of endocrinology clinic patients revealed that 57% of patients aged 55 and older presenting with primary hypothyroidism carried a diagnosis of autoimmune thyroiditis, while 32% carried a diagnosis of postsurgical hypothyroidism and 12% had a diagnosis of post-radioiodine hypothyroidism (). Only 2% of the patients in this referral population presented with documented evidence of secondary hypothyroidism. The incidence of post-ablative hypothyroidism has been noted to be higher in patients aged 55 and older (). The annual incidence of post-ablative hypothyroidism in this population is estimated to be 8%, with 12% of patients presenting with evidence of thyroid failure in the first year after undergoing treatment with radioactive iodine (,). The incidence of postsurgical hypothyroidism following subtotal thyroidectomy for treatment of hyperthyroidism has been estimated to be 16-27%, with 19% of patients presenting with evidence of thyroid failure in the first year after surgery (). External beam radiation therapy for treatment of head and neck malignancies has been associated with a high incidence of primary hypothyroidism. Up to 28% of patients treated with this modality eventually develop primary hypothyroidism at a median time of 15 months after completion of radiotherapy (). The risk of developing thyroid failure in this setting increases with advancing age. Elderly patients developing hypothyroidism may present with classic symptoms, but complaints are generally even less specific than those reported by younger patients presenting with evidence of thyroid hormone deficiency (–). In part this may be due to patients and physicians ascribing nonspecific complaints to other comorbid disorders common among the elderly, or to the effects of aging itself (). A study that compared the frequency of 24 symptoms of hypothyroidism reported by elderly and nonelderly patients found that complaints of fatigue and weakness were reported by more than 50% of elderly patients, but that significantly fewer complaints were reported by the elderly compared to a nonelderly group (). Elderly patients less often complained of cold intolerance, weight gain, paresthesias, and muscle cramps. Evaluation of a questionnaire administered to patients newly diagnosed with hypothyroidism ascribed to autoimmune thyroiditis showed that while all 13 referable symptoms were more prevalent in subjects younger than 60 years of age, the only referable symptoms that were more prevalent in older subjects were fatigue, dyspnea, and wheezing (). Other neurological symptoms that have been reported to occur more commonly in older patients include hypogeusia and dysgeusia, impaired hearing, and ataxia. Physical findings evident in hypothyroid elderly individuals may include bradycardia, diastolic hypertension, pallor, dry skin, coarse hair, hoarseness, dysarthria, delayed relaxation of deep tendon reflexes, and mental status changes (). The severity of specific findings may be exacerbated by comorbid cardiovascular, neuropsychiatric, dermatologic, or rheumatologic conditions that are more common among the elderly (). In some cases it may be necessary to evaluate responses to thyroid hormone replacement to determine the extent to which certain findings represent manifestations of thyroid hormone deficiency. Morphologic changes in the size and appearance of the thyroid do not appear to increase with aging (). Elderly patients with autoimmune thyroiditis are more likely to present with the atrophic form of the disorder without goiter (). Neuropsychological testing of elderly patients with hypothyroidism has demonstrated that they score lower on Mini-Mental Status Tests and on 5 of 14 specific indices of visual-spatial function, memory, word fluency, attention, and psychomotor function (). Analysis of laboratory test results has demonstrated that 54% of patients diagnosed with hypothyroidism have increased serum creatinine levels that may be correlated with advancing age (). Pericardial effusion is one of the few radiographic findings associated with hypothyroidism, but the true incidence of this complication appears to be lower than previously estimated (). Severe medical complications of hypothyroidism are more common in affected elderly persons. The majority of patients presenting with myxedema coma are elderly. Elderly patients with unrecognized hypothyroidism may be at greater risk for the development of perioperative and intraoperative complications. One study that compared patients with unrecognized hypothyroidism with controls matched for age, sex, and operative procedure identified higher rates of intraoperative hypotension, heart failure, and postoperative gastrointestinal and neuropsychiatric complications in hypothyroid patients (). A prospective study that screened hospitalized patients aged 60 and older for thyroid dysfunction reported that unrecognized overt hypothyroidism in this population may be associated with significantly higher mortality (). Accurate diagnosis of primary hypothyroidism in the elderly relies primarily, as it does in all patients, on the measurement of a sensitive serum TSH level. Although data from the NHANES III study has established that median TSH levels appear to increase with advancing age, the normal upper limit of an established reference range may still be used as a cutoff to confirm the diagnosis of primary hypothyroidism in most elderly patients. While a blood spot TSH level has been shown to be an adequate screening test for the detection of overt primary hypothyroidism in the elderly, it may not be sensitive enough to detect cases of subclinical hypothyroidism characterized by elevated serum TSH levels with normal T4 or free T4 levels (). One study has determined that there may be a negative correlation between age and the degree to which TSH levels are elevated in elderly patients presenting with primary hypothyroidism (). In cases of suspected secondary hypothyroidism that may result from disruption of the anatomy or function of the hypothalamic-pituitary axis, the TSH level may not be relied upon as an accurate index of thyroid function. In this setting the free T4 level may serve as more reliable measure of thyroid hormone production. The interpretation of thyroid function test profiles in hospitalized or institutionalized patients must be tempered by an understanding of how nonthyroidal illnesses may produce changes in TSH and thyroid hormone levels (). The direction and extent of changes observed may depend on the severity of an underlying illness and the point in the course of recovery at which thyroid function tests are measured (). Longitudinal studies have demonstrated that early on in the course of severe illnesses or protracted procedures, TSH levels in euthyroid patients may decline to levels that fall below the lower limits of normal reference ranges (). This change may be paralleled by a decline in T4 and T3 levels that may be particularly pronounced in elderly patients. One study demonstrated that 59% of elderly patients known to be euthyroid had documented low T3 levels measured during a course of hospitalization, whereas another demonstrated that changes in T3 levels detected in elderly hospitalized patients were more closely correlated with the severity of each underlying illness than with advanced age itself (,). Studies have demonstrated a correlation between declining T4 levels and increasing mortality rates in critical care patients (). Free T4 levels measured by equilibrium dialysis or ultrafiltration methods, if they are within reference ranges, may help to distinguish hypothyroidism from the effects of altered thyroid hormone binding that may occur in critically ill patients (). Current data indicates that the normal or low TSH levels found in the presence of low T4 and T3 levels in the setting of nonthyroidal illness likely reflect the combined effects of central hypothyroidism and reduced peripheral generation of T3, effectively representing a deficiency of thyroid hormone. Whether this condition should be treated with administration of thyroid hormone preparations remains controversial. Some observers argue in favor of thyroid hormone replacement, while others weigh against it, without conclusive data to support either viewpoint (,). If a patient survives to recover from nonthyroidal illness, TSH levels may transiently rise above the upper limits of reference ranges (). If thyroid function tests are checked when a transiently increased TSH level precedes increases in low T4 and/or T3 levels, the profile that emerges may appear to be consistent with primary hypothyroidism (). This could lead to unnecessary treatment with thyroid hormone, which would probably be inconsequential. In cases where changes in TSH and thyroid hormone levels may be plausibly ascribed to nonthyroidal illness, the patient’s thyroid function tests should be reassessed one to two weeks later to see if observed changes are resolving. One study that tracked thyroid function test profiles in hospitalized elderly female patients showed that while 14% of the subjects had increased TSH levels and decreased T4 and T3 levels on initial assessment, only 2% were proven to have evidence of underlying primary hypothyroidism during follow up (). Measurement of anti-thyroid antibody levels may help to confirm a suspected diagnosis of autoimmune thyroiditis as the underlying cause of primary hypothyroidism. However, the presence or absence of elevated anti-thyroid antibodies may not be an absolute indicator of the likelihood of eventual development of primary hypothyroidism in elderly individuals. One study that measured TSH and anti-microsomal antibody levels in healthy elderly adults showed that positive titers were detected in only 67% of subjects with TSH levels > 10.0 mIU/L and 18% of subjects with normal TSH levels (). A similar study that measured anti-thyroid antibody levels in nursing home residents detected positive titers in only 64% of the women and 32% of the men presenting with increased TSH levels (). Comparative measurements of anti-thyroglobulin, anti-microsomal, and anti-thyroid peroxidase antibodies have demonstrated that while there may be a similar prevalence of positive anti-microsomal and anti-thyroid peroxidase titers among elderly adults, mean values of anti-thyroid peroxidase antibody levels tend to be much more commonly elevated in this population (). Nonetheless anti-thyroid antibody measurements in the elderly may help to predict the likelihood of progression from subclinical to overt hypothyroidism (). Abnormalities in other routine laboratory test parameters may suggest possible undetected hypothyroidism. Hyponatremia caused by decreased free water excretion may complicate moderate and severe cases of primary hypothyroidism (). Hyperlipidemia characterized by hypercholesterolemia is commonly evident (). Cases of primary hypothyroidism that are severe enough to precipitate myopathy may present with increased creatine phosphokinase levels (). A hypochromic microcytic anemia that is not associated with any detectable hemoglobinopathy or iron deficiency state may be evident in up to 15% of cases of moderate primary hypothyroidism (). Homocysteine and lipoprotein (a) levels may be increased in patients with primary hypothyroidism, potentially contributing to an increased risk of atherosclerotic disease (). Initial treatment of hypothyroidism in elderly patients should typically start with sodium levothyroxine (thyroxine) administered in lower doses than those usually prescribed for healthy younger patients (e.g.0.25 to 0.5 mcg/kg/day). Once cardiovascular tolerance of a starting dose has been assessed, most experts recommend gradually increasing daily doses by 12.5-25 mcg every four to six weeks until adequate replacement is confirmed by repeat TSH measurement. The degree to which this general strategy has been adopted in practice was confirmed by a recent survey of members of the American Thyroid Association (). A recent trial demonstrated that older patients without any underlying cardiovascular disease could be safely started on full replacement doses of thyroxine (1.6 mcg/kg) without any adverse effects (). While a great deal of interest has arisen regarding the potential benefits of adding doses of liothyronine (T3) to thyroxine to approximate physiologic thyroid hormone secretion, a number of randomized trials have shown that this mode of treatment does not have any significant impact on identified symptoms, mood, cognitive function, or quality of life (–). Serial measurements of TSH levels four to six weeks after each change in thyroxine dosage should be used to monitor thyroid hormone replacement therapy. In a comparison trial based on a reference standard of measured TSH response to TRH administration, basal TSH levels proved to be more sensitive to fine alterations in thyroxine doses than basal free T4 or free T3 levels. Most experts recommend targeting a normal TSH range in elderly patients (). While 39% of ATA members recommended targeting a TSH range of 0.5-2.0 mIU/L when treating younger patients, a comparable number reported that they were generally more liberal in their approach to elderly patients, targeting TSH ranges of 1.0-4.0 mIU/L. Treatment with thyroxine has been shown to increase cognitive testing performance and reduce oro-cecal transit time from an average of 135 minutes in a hypothyroid state to 75-95 minutes with adequate replacement (,). While thyroid hormone supplementation to a level that completely corrects the hormonal deficiency may be an optimal goal, some patients with ischemic heart disease may not be able to tolerate full replacement doses of thyroxine (,). One study of patients with known coronary artery disease and primary hypothyroidism reported that precipitation of angina symptoms limited titration of thyroxine in two-thirds of cases, while precipitation of hypothyroid symptoms limited titration of antianginal agents in one-third of cases. Even with the addition of propranolol at maximally tolerated doses, 46% of the patients surveyed rated control of their angina and hypothyroid symptoms as fair to poor (). Thyroxine dose requirements in elderly patients may be related to several factors including declining metabolic clearance, progression of underlying thyroid failure, declining body mass, and interactions with other medications prescribed for the treatment of co-morbid conditions (,). On average, elderly patients with primary hypothyroidism receive initial daily doses that are 20 mcg lower and maintenance daily doses that are 40 mcg lower than those prescribed for younger and middle-aged patients (–). One study suggested that lean body mass may be a better predictor of daily replacement doses than age or weight alone (). Another reported that most of the age-dependent differences in thyroxine requirements noted might be attributed to the effects of chronic disease, since substantially lower average daily replacement doses were reported by elderly patients treated for other chronic medical disorders (). A study that tracked changes in elderly patients’ thyroxine requirements over time based on the etiology of their primary hypothyroidism reported that daily replacement doses increased in patients who initially presented with autoimmune thyroiditis or postsurgical hypothyroidism, decreased in patients who initially presented with post-ablative hypothyroidism, and did not change in patients who initially presented with subclinical hypothyroidism or drug-induced hypothyroidism (). In situations where cognitive or functional impairment may make it difficult for patients to comply with daily administration of thyroxine, alternative dosing schedules may be considered. A study that compared daily administration of thyroxine to twice weekly administration of comparable cumulative daily doses in elderly women showed that both regimens produced similar peak and trough free T4, T3, and TSH levels (). Trials of regimens based on once weekly administration of cumulative daily doses of thyroxine have demonstrated similar results without any evidence of precipitation of thyrotoxicosis (). A number of medications used to treat other comorbid conditions in the elderly may interfere with absorption and metabolism of thyroxine (). Ingestion of 2,000 mg of calcium carbonate has been shown to interfere with the peak and total incremental absorption of a concomitantly administered treatment dose of thyroxine (). Ferrous sulfate, sucralfate, aluminum hydroxide, cholestyramine, colestipol, and raloxifene have also been reported to impair absorption of thyroxine (,). In postmenopausal women with primary hypothyroidism, treatment with estrogen replacement therapy may lead to increased thyroxine dose requirements as a consequence of increased production of thyroid binding globulin (TBG) (). Women with hormonally-responsive breast cancer who receive fluoxymesterone may require substantially lower doses of thyroxine during courses of treatment, as exposure to this androgenic steroid may decrease effective TBG production (). Long-term administration of phenytoin, carbamazepine, phenobarbital, or rifampin in the setting of treated primary hypothyroidism typically increases metabolism of thyroxine, increasing the dose of thyroxine required to provide optimal replacement (–). Overtreatment with excessive doses of thyroxine may be associated with significant morbidity in the elderly. Palpitations, anxiety, tremulousness, irritability, insomnia, heat intolerance, hyperdefecation, and weight loss may be precipitated or exacerbated by iatrogenic thyrotoxicosis. In elderly patients, exposure to excessive amounts of thyroid hormone may be associated with increased risks of atrial fibrillation, other tachyarrhythmias, and progressive declines in bone mineral density (). A prospective study of the incidence of atrial arrhythmias in patients aged 60 and older determined that over the course of a 10-year period, the relative risk of development of new-onset atrial fibrillation in subjects with initial TSH levels < 0.1 mIU/L was 3.1 when compared to subjects with normal TSH levels (). Further analysis revealed that suppressed TSH levels identified in 77% of these subjects were attributable to iatrogenic thyrotoxicosis resulting from overtreatment. A study that tracked bone mineral density changes in women treated with thyroxine documented greater mean rates of decline in the lumbar spines of those with suppressed TSH levels (). A recent cohort study that tracked TSH and free T4 and T3 levels in healthy aging adults in tandem with inventories of medication use reported that half of the cases of prevalent and incident thyrotoxicosis identified could be attributed to over-treatment with levothyroxine (). Mild or subclinical hypothyroidism, which is characterized by an increased TSH level with concomitant free thyroid hormone levels that fall within normal limits, is very common among elderly men and women. The estimated prevalence of this condition has varied from 4-15%. A study evaluating a community of healthy elderly adults in the southwest of France reported that 4.2% of subjects presenting with increased TSH levels had normal free T4 levels (). Within this group, mild hypothyroidism was linked with an increased prevalence of symptoms of depression. A study that evaluated thyroid function profiles in a bi-ethnic urban community reported that mild hypothyroidism was more commonly identified in females and non-Hispanic white subjects than Hispanic subjects (). Stratified analysis of the impact of mild hypothyroidism in this population revealed no significant alterations in health status measures in subjects with TSH levels ranging between 4.7-10.0 mIU/L. A study that inventoried clinical findings of hypothyroidism in a population of geriatric clinic patients reported that while 15.4% of the men and 14.6% of the women screened met criteria for mild hypothyroidism, the incidence of symptoms and signs consistent with thyroid hormone deficiency detected in these subjects was similar to that reported for euthyroid subjects (). An array of studies that have tracked changes in thyroid function in cohorts of aging subjects in the United States, Australia, the Netherlands, Spain, the United Kingdom, and China have reported that the development of hypothyroidism in elderly patients does not appear to be associated with any change in cognitive function, increased levels of depression, or diminished ability to perform activities of daily living (–). A study that measured an array of anthropometric, biochemical, and neuropsychiatric parameters in Korean subjects aged 65 years and older showed that subclinical hypothyroidism did not appear to be associated with any discernible metabolic or neuropsychiatric derangements (). A study that evaluated subgroups of subjects enrolled in the Health, Aging, and Body Composition study found that those determined to have mild subclinical hypothyroidism (defined by a TSH level of 4.5-7.0 mIU/L with normal thyroid hormone levels) demonstrated better mobility, cardiorespiratory fitness, and walking ease than subjects who were euthyroid or determined to have moderate subclinical hypothyroidism (defined by a TSH level of 7.0-20.0 with normal thyroid hormone levels) (). An analysis of subgroups in this cohort study identified increased odds of prevalent metabolic syndrome among subjects with TSH levels > 10 (). A study that evaluated postmenopausal women at risk for development of osteoporosis reported that subclinical hypothyroidism was not associated with decreased bone mineral density or an increased risk of vertebral or non-vertebral fracture (). Several longitudinal studies have tracked the natural history of untreated mild hypothyroidism in elderly persons. A study of nursing home residents confirmed that over time TSH levels declined to normal ranges in 51% of subjects with initial TSH levels that were lower than 6.8 mIU/L (). Serial TSH levels were persistently elevated in the remainder of these subjects and in all subjects with initial TSH levels greater than 6.8 mIU/L. A similar study that stratified subjects on the basis of anti-thyroid antibody levels reported that 80% of elderly adults with mild hypothyroidism with initial measured anti-microsomal antibody titers greater than 1:1,600 eventually progressed to develop overt hypothyroidism requiring treatment with thyroxine replacement therapy (). A study that tracked 505 subjects diagnosed with mild hypothyroidism over time showed that positive anti-thyroid peroxidase antibodies and higher total cholesterol levels measured at baseline were associated with increased odds of eventual progression to overt hypothyroidism (). Two studies showed that when elderly patients diagnosed with subclinical hypothyroidism were tracked over a span of 4-4.2 years, 44-54% demonstrated normalization of TSH levels consistent with reversion to a euthyroid state (,). Findings that were associated with reversion included lower baseline TSH levels, homogenous echotexture of thyroid tissue on ultrasound imaging, and an absence of detectable anti-thyroid peroxidase antibodies. Questions have been raised about the possible association of mild hypothyroidism with an increased risk of cardiovascular disease in the elderly. One study that confirmed the presence of mild hypothyroidism in 10.8% of subjects drawn from a cohort of postmenopausal women reported a greater age-adjusted prevalence of coronary and aortic atherosclerosis in mildly hypothyroid women (). Even stronger associations between mild hypothyroidism and atherosclerotic disease were noted among postmenopausal women with elevated anti-thyroid antibody levels. Another study that evaluated the prevalence of peripheral vascular disease among nursing home residents reported that 78% of subjects with mild hypothyroidism presented with reproducible claudication, whereas symptomatic peripheral vascular disease was only identified in 17% of euthyroid subjects (). A study that evaluated thyroid function in patients enrolled in a study of pre-existing heart failure reported that subclinical hypothyroidism presenting with TSH levels ≥ 7 mIU/L was associated with an increased risk of a need for the use of ventricular assist devices, heart transplantation, and death (). Population-based studies that have tracked thyroid function in elderly subjects have reported differing results regarding risks of cardiovascular disease. A study that examined community-dwelling subjects aged 70-79 years enrolled in the Health, Aging, and Body Composition study found that subclinical hypothyroidism was associated with an increased incidence of congestive heart failure (). A study that examined subjects aged 65 years and older enrolled in the Cardiovascular Health study found that subclinical hypothyroidism was not associated with an increased incidence of coronary artery disease, cerebrovascular disease, cardiovascular mortality, or all-cause mortality (). Analysis of subgroup data tracked over the course of 12 years and echocardiographic parameters tracked over the course of 5 years demonstrated that subjects with TSH levels ≥10.0 mIU/L had a higher incidence of heart failure events, a greater increase in left ventricular mass, and appreciable changes in measurements reflecting changes in diastolic function compared to euthyroid subjects (). Two meta-analyses that analyzed data from a range of prospective cohort studies incorporating measurements of thyroid function identified a modest increase in the risk of coronary artery disease and associated mortality in subjects determined to have evidence of subclinical hypothyroidism (,). More recent analyses of subgroups tracked in cohort studies have reported that persistent subclinical hypothyroidism does not appear to be associated with an increased risk of all-cause mortality, cardiovascular mortality, coronary artery disease, myocardial infarction, or congestive heart failure (–). An analysis of NHANES III data has identified increased mortality in subjects diagnosed with concurrent subclinical hypothyroidism and congestive heart failure, and a retrospective cohort study from Israel involving 17,440 patients with subclinical thyroid disease showed that TSH levels > 6.35 mIU/L were associated with increased mortality (,). Consideration of treatment of mild hypothyroidism in the elderly is often predicated on the notion that restoration of normal thyroid hormone levels might help to relieve symptoms that could be exacerbated by a deficiency of thyroid hormone. The Thyroid Hormone Replacement for Untreated Older Adult with Subclinical Hypothyroidism (TRUST) trial was specifically designed to address this question (). It randomized 737 subjects ≥ 65 years of age with persistent subclinical hypothyroidism to double-blinded placebo-controlled administration of doses of thyroxine adjusted to normalize TSH levels. Assessment based on a thyroid-related quality-of-life questionnaire after one year of treatment showed no difference in hypothyroid symptom scores or tiredness scores. An analysis that combined data from 146 TRUST trial subjects ≥ 80 years of age with data from 145 subjects enrolled in the Institute for Evidence-Based Medicine in Old Age 80-plus trial who were evaluated with a similar protocol also showed no improvement in hypothyroid symptoms or fatigue; however, a majority of those with elevated TSH levels had values below 7 mIU/L (). The attendant risks of iatrogenic thyrotoxicosis in elderly individuals must be taken into account when weighing the potential risks and benefits of thyroid hormone replacement (). Partial or complete reversibility of hypercholesterolemia has been shown to accompany thyroxine treatment of mild hypothyroidism in the majority of small interventional trials addressing this issue (). Lowering of lipoprotein (a) levels has been shown in some, but not all studies (). Hyperhomocysteinemia in patients with mild hypothyroidism has not been shown to be reversed with thyroxine therapy. A nested trial incorporated in the TRUST trial showed that normalization of TSH levels with levothyroxine for a span of one year did not have any impact on carotid intima media thickness or carotid atherosclerosis (). Patients with severe hypothyroidism may present in a state of pronounced multisystem failure termed myxedema coma (,). Elderly patients with untreated or undertreated primary hypothyroidism and comorbid disorders may be particularly susceptible to decompensation that leads to onset and progression of this life-threatening condition (,). In addition to coma, there may be hypothermia, bradycardia, hypotension, congestive heart failure, ileus, and hypoventilation with hypercapnia and respiratory acidosis. In situations where historical information may be unobtainable, physical examination may reveal evidence of prior thyroid surgery, laryngeal surgery, or head and neck external beam radiation therapy. Radiographic studies may reveal pericardial effusions, which may also be reflected in low voltage waves on electrocardiograms. Although such pericardial fluid collections may be large, they are usually not hemodynamically significant. Laboratory evaluation confirming severe hypothyroidism may also reveal evidence of hyponatremia, hypoglycemia, and/or adrenal insufficiency. Myxedema coma is an endocrine emergency with a mortality rate that may approach 40% (). In addition to older age, factors that may be associated with an increased risk of mortality include comorbid cardiovascular disease and treatment with high-dose thyroxine replacement therapy (). Generally recommended supportive measures include critical care-level monitoring of vital signs, careful external rewarming with heating blankets, correction of fluid and electrolyte imbalances, avoidance of hypnotics and sedatives, empiric treatment of suspected underlying infections, and mechanical ventilatory support as indicated. Given the theoretical risk of concomitant adrenal insufficiency due to polyglandular autoimmune syndromes or hypothalamic-pituitary compromise, many experts recommend empiric treatment with stress-dose glucocorticoids until definitive stimulatory testing can be performed. Recommendations regarding the dose and composition of thyroid hormone preparations that should be administered to treat myxedema coma differ. Most experts concur that intravenous thyroxine should be used to circumvent impaired gastrointestinal absorption. Some have recommended initial thyroxine loading doses, while others have advocated co-administration of liothyronine (T3). Treatment of critically ill hypothyroid patients with high-dose thyroxine has been associated with a significant increase in cardiac index due to increased heart rate and stroke volume with decreased systemic vascular resistance (). Although the onset of action of liothyronine is more rapid than thyroxine, supraphysiologic T3 levels measured after treatment have been correlated with increased mortality in older patients presenting with myxedema coma (). A judicious approach may involve administration of a loading dose of 200-300 mcg of intravenous thyroxine followed by administration of 50 mcg daily. Depending on the estimated risk of underlying cardiovascular disease, a loading dose of 5-25 mcg of liothyronine may be administered concomitantly followed by doses of 2.5-5 mcg every eight hours until clinical improvement is evident. Intravenous hydrocortisone may be administered in stress doses of 50-100 mg every 8 hours while testing for underlying adrenal insufficiency is performed. Professional organizations and task forces have issued a range of recommendations concerning the advisability and timing of biochemical screening for hypothyroidism in adult populations () (–). Screening Recommendations for Hypothyroidism in Adults

Guideline Methods used to analyze evidence Organization Year of publication
American Thyroid Association guidelines for the detection of thyroid dysfunction Narrative literature review Expert opinion American Thyroid Association 2000
Consensus statement for good practice and audit measures in the management of hypothyroidism and hyperthyroidism Narrative literature review Expert opinion Royal College of Physicians of London Society for Endocrinology 1996
Laboratory medicine practice guideline for the diagnosis and monitoring of thyroid disease testing Narrative literature review Expert opinion American Association of Clinical Chemists American Association of Clinical Endocrinologists American Thyroid Association Endocrine Society National Academy Clinical Biochemistry 1990, in progress
Periodic health examinations: summary of AAFP policy recommendations & age charts Based on systematic review performed by US Preventive Services Task Force Expert opinion American Academy of Family Physicians 1996, 2001
Screening for thyroid disease Systematic review Meta-analysis of observational trials American College of Physicians – American Society of Internal Medicine 1997
Screening for thyroid disease Systematic review US Preventive Services Task Force 1996
AACE clinical practice guidelines for the evaluation and treatment of hyperthyroidism and hypothyroidism Narrative literature review Expert opinion American Association of Clinical Endocrinologists American College of Endocrinology 1996
Treatment guidelines for patients with hyperthyroidism and hypothyroidism Narrative literature review Expert opinion American Thyroid Association 1995, 1999
Screening for thyroid disorders and thyroid cancer in asymptomatic adults Systematic review Canadian Task Force on Preventive Health Care 1994, 1999

A panel of invited experts representing the American Thyroid Association, the American Association of Clinical Endocrinologists, and the Endocrine Society at a consensus development conference found a paucity of evidence regarding the morbidity and impact of subclinical thyroid disease, as well as the potential complications of instituting therapy.

  1. Consequently, this panel concluded that there was insufficient evidence to support routine population-based screening of asymptomatic adults.
  2. However, the panel did conclude that the weight of available evidence supported the adoption of aggressive case-finding strategies in patients at high risk for the development of hypothyroidism.

Specific groups identified as being at increased risk for thyroid dysfunction include women aged 60 years and older and patients with histories of atrial fibrillation, thyroid surgery, radioactive iodine treatment, external beam radiation therapy, or family members with confirmed thyroid disease.

  • A guideline issued by the American College of Physicians states that it is reasonable to check TSH levels in women aged 50 years and older presenting with symptoms that may be consistent with thyroid dysfunction, given the high prevalence of undiagnosed thyroid disorders among that population (–).
  • The Policy Recommendations for the Periodic Health Exam published by the American Academy of Family Physicians take a more neutral stance, recommending against routine screening in patients less than 60 years old without any specific provisions ().

The United States Preventive Services Task Force and the Canadian Task Force on the Periodic Health Examination have both concluded that there is not enough evidence regarding the impact of diagnosis and treatment of detectable thyroid disease to rule for or against routine screening of asymptomatic adults (,).

  1. Utility analysis based on decision modeling has demonstrated that routine periodic screening for mild hypothyroidism may become more cost-effective with increasing age ().
  2. Studies focusing on actual screening of identified populations of elderly adults have reported mixed results.
  3. One study reported that selection of candidates based on body mass index, symptoms consistent with thyroid dysfunction, or a family history of thyroid disease failed to identify the majority of elderly patients eventually confirmed to have elevated or suppressed TSH levels ().

Another study that evaluated elderly patients presenting with suspected dementia revealed that hypothyroidism was the second most common undiagnosed disorder contributing to cognitive impairment (). A similar study reported that measurement of TSH levels identified hypothyroidism in 3.6% of elderly adults presenting for evaluation of mental status changes ().

  • Screening studies involving hospitalized patients reported that 2.3% of geriatric inpatients and 11.2% of patients admitted for elective cardiac surgery had thyroid function profiles consistent with hypothyroidism ().
  • These findings are not surprising in light of the substantial prevalence of hypothyroidism among elderly patients in general.

An analysis of profiles of TSH and thyroid hormone levels tracked in subjects enrolled in the Birmingham Elderly Thyroid Study reported high stability of euthyroid and subclinical hypothyroid indices over a 5 year interval, indicating that repeat testing may not be warranted in this population ().1.

Hollowell JG, Staehling NW, Flanders WD, Hannon WH, Gunter EW, Spencer CA, Braverman LE. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III).J. Clin. Endocrinol. Metab.2002; 87 (2):489–499.2.3. Tunbridge WM, Evered DC, Hall R, Appleton D, Brewis M, Clark F, Evans JG, Young E, Bird T, Smith PA.

The spectrum of thyroid disease in a community: the Whickham survey. Clin. Endocrinol. (Oxf).1977; 7 (6):481–493.4. Sawin CT, Castelli WP, Hershman JM, McNamara P, Bacharach P. The aging thyroid. Thyroid deficiency in the Framingham Study. Arch. Intern. Med.1985; 145 (8):1386–1388.5.

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  3. A randomized study in a Norwegian rural community (Naerøy).
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  6. Thyroid dysfunction in adults over age 55 years.
  7. A study in an urban US community.

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The Colorado thyroid disease prevalence study. Arch. Intern. Med.2000; 160 (4):526–534.9. Bemben DA, Winn P, Hamm RM, Morgan L, Davis A, Barton E. Thyroid disease in the elderly. Part 1. Prevalence of undiagnosed hypothyroidism. J Fam Pract.1994; 38 (6):577–582.10. Drinka PJ, Nolten WE. Prevalence of previously undiagnosed hypothyroidism in residents of a midwestern nursing home.

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JAMA.1989; 261 (18):2653–2655.13. Surks MI, Hollowell JG. Age-specific distribution of serum thyrotropin and antithyroid antibodies in the US population: implications for the prevalence of subclinical hypothyroidism.J. Clin. Endocrinol. Metab.2007; 92 (12):4575–4582.14. Kung AW, Janus ED. Thyroid dysfunction in ambulatory elderly Chinese subjects in an area of borderline iodine intake.

Thyroid.1996; 6 (2):111–114.15. Szabolcs I, Podoba J, Feldkamp J, Dohan O, Farkas I, Sajgó M, Takáts KI, Góth M, Kovács L, Kressinszky K, Hnilica P, Szilágyi G. Comparative screening for thyroid disorders in old age in areas of iodine deficiency, long-term iodine prophylaxis and abundant iodine intake.

Clin. Endocrinol. (Oxf).1997; 47 (1):87–92.16. Dayan CM, Daniels GH. Chronic autoimmune thyroiditis. The New England journal of medicine.1996; 335 (2):99–107.17. Mariotti S, Chiovato L, Franceschi C, Pinchera A. Thyroid autoimmunity and aging. Exp. Gerontol.1998; 33 (6):535–541.18. Pinchera A, Mariotti S, Barbesino G, Bechi R, Sansoni P, Fagiolo U, Cossarizza A, Franceschi C.

Thyroid autoimmunity and ageing. Horm. Res.1995; 43 (1–3):64–68.19. Díez JJ. Hypothyroidism in patients older than 55 years: an analysis of the etiology and assessment of the effectiveness of therapy.J. Gerontol. A Biol. Sci. Med. Sci.2002; 57 (5):M315–320.20.

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Is hyperthyroidism a lifelong disease?

For many people, hyperthyroidism is a chronic, or lifelong, condition. Once it’s treated, you must recheck your thyroid levels to ensure you’re getting the correct amount of medication.

Can you get over thyroid disease?

Hyperthyroidism is treatable. Some causes may go away without treatment. Hyperthyroidism caused by Graves disease usually gets worse over time. It has many complications, some of which are severe and affect quality of life.