How does t3 and t4 affect metabolism

TH plays a significant role in energy expenditure through both central and peripheral actions. TH maintains basal metabolic rate, facilitates adaptive thermogenesis, modulates appetite and food intake, and regulates body weight. Basal metabolic rate BMR is the primary source of energy expenditure in humans, and reductions in BMR can result in obesity and weight gain TH is a key regulator of BMR, but the targets are not clearly established BMR correlates with lean body mass and thyroid hormone levels 52 , Cold and heat intolerance are hallmark clinical features of patients with hypothyroidism and hyperthyroidism, respectively.

In addition, resting energy expenditure REE is remarkably sensitive to TH, especially in athyreotic individuals 4.

TH stimulates metabolic cycles involving fat, glucose, and protein catabolism and anabolism, but these are minor contributions to BMR. TH maintains BMR by uncoupling oxidative phosphorylation in the mitochondria , or reducing the activity of shuttle molecules that transfer reducing equivalents into the mitochondria 72 , In skeletal muscle, TH increases the leak of protons through the mitochondrial inner membrane, stimulating more oxidation to maintain ATP synthesis, since the proton-motive force driving ATP production is compromised.

The presence of uncoupling protein UCP 2 and 3 in skeletal and cardiac muscle initially suggested that these proteins were mediators of the TH-stimulated proton leak. Further investigation revealed that TH treatment produced upregulation of UCP2 and UCP3, but this was not associated with changes in the proton gradient in human muscle Clinically, when transitioning from hypothyroidism to euthyroidism, TH induced energy expenditure results in heat production without a significant increase in ATP generation.

In hyperthyroidism, there is an increase in both ATP synthesis and heat production T 3 also regulates the efficiency of ATP synthesis induction of mitochondrial glycerolphosphate dehydrogenase mGPD , a shuttle enzyme that contributes to the generation of ATP by transferring reducing equivalents generated in the cytoplasm into the mitochondrial membrane. Mice homozygous for a GPD gene knockout have higher levels of T 4 and T 3 and impaired ability to maintain core body temperature, consistent with a defect in thermogenesis T 3 induction of UCP3 in skeletal muscle may play a role in thermogenesis.

In mice lacking beta 1, 2, and 3 adrenergic receptor beta-less , which are cold intolerant, T 3 treatment during cold exposure resulted in maintenance of body temperature T 3 treatment of UCP3 knockout mice, compared with wild-type, had slightly less thermogenesis, indicating that T 3 induction of UCP3 may be important for thermogenesis in some settings Homeothermic species have developed a nonshivering or facultative thermogenesis to maintain core body temperature after cold exposure and increase energy expenditure after eating.

The primary site of this adaptive thermogenesis in rodents is in BAT Hypothyroid rodents develop marked hypothermia with cold exposure, and T 4 treatment reverses this via induction of BAT activity This demonstrates TR isoform specificity in metabolic regulation within a single tissue, and both TR isoforms are required for a normal thermogenic response.

UCP1 expression is critical to BAT thermogenesis, although it is now well established that D2 activity, required for the local conversion of T 4 to T 3 , is also essential D2KO mice develop hypothermia and must rely on shivering to maintain core body temperature In addition, with cold exposure, D2KO mice preferentially oxidize fat.

They are resistant to diet-induced obesity and have normal glucose tolerance due to increased sympathetic tone. The evaluation of D2 knockout mice provided an important insight into difference between rodents and humans with respect to the thermoneutral temperature. There is both visceral and subcutaneous BAT in humans, which may have specific functions that relate to the anatomical location Until recently, human BAT was considered to be important in neonates, but not likely to be important in the adult.

In general, there is more BAT in younger and leaner individuals, and it is induced by cold. A recent study showed that direct biopsy of adipose tissue from the supraclavicular areas, thought to contain BAT tissue, had increased oxidative capacity and increased expression of UCP-1 Skeletal muscle has been recognized as a key TH target for contractile function, regeneration, and transport as well as for metabolism and glucose disposal , TH stimulation favors transition to fast-twitch fibers and transition to a faster myosin heavy chain MHC form.

The significant regulation of D2 is a key factor that modulates T 3 levels in skeletal muscle. In skeletal muscle development and regeneration after injury, FoxO3 stimulates D2 expression Skeletal muscle injury is associated with a twofold increase in local T 3 levels, not seen in D2 knockout animals. There has also been interest in the common Myf 5 expressing precursor cell for both skeletal muscle and brown adipose tissue The zinc finger protein, PRDM16, directly represses white fat genes and activates brown fat genes D2 levels are higher in slow-twitch compared with fast-twitch muscle fibers and are stimulated by hypothyroidism, but not by cold exposure It is well established that thyroid status, either hypothyroidism or hyperthyroidism, is associated with changes in weight and REE.

In healthy individuals, variations in serum TSH, even within the reference range, are associated with body weight and body weight change in both men and women 80 , Interestingly, reestablishing euthyroidism with T 4 treatment is associated with reductions in body weight and increase in REE in hypothyroid individuals, but fat mass is unchanged and weight loss is primarily excretion of excess body water It is possible that increased caloric intake, stimulated by TH, is responsible for this discrepancy.

In addition, given the impact of central regulation of TH on orexigenic neuropeptides 78 , variable regulation of the HPT axis with altered leptin levels also could be responsible for this metabolic abnormality Hyperthyroid patients have increased intake of carbohydrates, which reverses after treatment of the hyperthyroidism The stimulation of a preference for carbohydrate intake is thought to be due to central adrenergic stimulation.

A study comparing treatment of hypothyroid patients with T 3 or T 4 monotherapy showed that T 3 treatment resulted in significant weight loss and reduction in total cholesterol and apolipoprotein B, compared with T 4 treatment, without adverse cardiovascular outcomes This study also noted a nonsignificant trend effect in decreasing fat mass with T 3 therapy.

While there was no significant change in REE, it is likely that the weight reduction seen in T 3 therapy is a result of an increase in metabolic rate. The greatest weight change associated with thyroid disease is the body weight increase seen after treatment of hyperthyroidism Most patients regain more weight than they had prior to having Graves' disease, sustaining the higher energy intake associated with hyperthyroidism, even when they become euthyroid.

This study also examined body composition and found that weight loss in hyperthyroidism was due to loss of both fat and lean body mass. The metabolic activity of fat is also becoming increasingly recognized and is a significant site of TH action Lipid homeostasis in liver is coordinately regulated by direct actions of T 3 and indirect crosstalk with nutrient-activated nuclear receptors.

HMG-CoA reductase is subject to feedback inhibition by cholesterol. This then reduces cholesterol synthesis. CYP7a1 is a rate-limiting enzyme in bile acid synthesis.

TR directly stimulates CYP7a1 gene expression in human liver. This regulation is mediated by similar DR4 response elements in these gene promoters. Phosphoenolpyruvate carboxykinase PEPCK catalyzes the key step initiating gluconeogenesis and is regulated by hormones at the transcriptional level, including T 3. In the presence of glyceraldehydephosphate G-3P , triglyceride is synthesized and transported to adipocytes.

When energy is needed, there is central activation of the sympathetic nervous system and release of catecholamines, which acts on adipocytes to hydrolyze TG. TH regulates cholesterol synthesis through multiple mechanisms.

A major pathway is TH stimulation of transcription of the LDL-R gene resulting in increased uptake of cholesterol and enhanced cholesterol synthesis This has been a major pathway of T 4 -mediated cholesterol lowering after T 4 treatment of patients with hypothyroidism SREBP-2 is a member of a family of transcription factors that regulate glucose metabolism, fatty acid synthesis, and cholesterol metabolism.

TH also reduces cholesterol through non-LDL receptor-mediated pathways. Mice with hypercholesterolemia due to LDL-receptor gene knockouts were treated with high dose T 3 or 3,5-diiodo- l -thyronine T 2 Under these conditions, the reduction in LDL-cholesterol was linked to reductions in apolipoprotein apo B48 and apoB Hepatic triglyceride production was increased.

The high doses of T 2 used were associated with cardiac toxicity and increased heart weight, but these findings suggest mechanisms for T 3 , in addition to stimulation of the LDL-receptor, for cholesterol lowering. Reverse cholesterol transport is a complex process that results in transfer of cholesterol to the liver for elimination as bile acids or neutral steroids.

The conversion of cholesterol to bile acids is required to maintain cholesterol homeostasis. This cholesterol clearance pathway is regulated by a number of nuclear receptors that control the expression of cholesterol 7-hydroxylase CYP7a1 , the rate-limiting step in bile acid synthesis Human and murine CYP7a1 are regulated by different nuclear receptors and their ligands Bile acids bind the TGR5 receptor on enteroendocrine L cells in the small intestine, which stimulates production of the incretin GLP-1 improving insulin sensitivity and increasing satiety.

In BAT, as previously described, bile acids bind TGR5 and stimulate expression of D2 increasing energy expenditure and promoting resistance to diet-induced obesity , Bile acids combine with the nuclear FXR receptor and stimulate target genes regulating cholesterol and bile acid metabolism A recent clinical study in both healthy and cirrhotic subjects revealed that bile acid synthesis correlated positively with energy expenditure, and postprandially, serum TSH decreased in both groups , suggesting that the bile acid serum level influences the thyroid pituitary axis set point.

Activation of FXR by bile acids also improves diabetes in animal models. An FXR knockout mouse model resulted in glucose intolerance and insulin insensitivity Treatment of diabetic mice with a synthetic FXR agonist repressed hepatic gluconeogenesis and enhanced liver sensitivity to insulin Bile acids, like thyroid hormone, impact the metabolism of lipids and glucose and are linked by activation of D2 in specific tissues.

TH stimulates both lipolysis and lipogenesis, although the direct action is lipolysis with lipogenesis thought to be stimulated to restore fat stores A time course study in rats carefully measured whole body lipid content and thermogenesis after T 3 treatment and concluded that the TH-induced lipogenesis is primarily to maintain fat loss that occurs with TH-induced lipolysis Fatty acids produced from TH-induced lipolysis are the substrate for the increase in thermogenesis T 3 regulation of these divergent metabolic pathways is subject to nuclear receptor crosstalk, ligand-binding, nutritional status, and competition for RXR heterodimers TH plays a significant role in the conversion of preadipocytes to adipocytes Another in vivo study demonstrated nuclear crosstalk via treatment with polyunsaturated fatty acids.

Impairment of this process is associated with hepatic steatosis and insulin resistance There is significant evidence for nuclear hormone crosstalk in the development and treatment of hepatic steatosis. In a gene expression array study of human hepatic steatosis samples, there was downregulation of T 3 -responsive genes in the steatosis samples compared with normal liver GC1 treatment was associated with increased endogenous glucose production and KB with reduced insulin-stimulated glucose uptake in skeletal muscle due to reduced GLUT4 expression.

Transgenic mice overexpressing FGF21 in liver have reduced plasma triglyceride concentrations and are resistant to weight gain after high-fat feeding. In a study of serum FGF levels in obese youth with steatohepatitis, FGF levels were elevated compared with control and correlated with hepatic fat content In these patients with obesity and liver damage, the elevated FGF levels may not be adequate to increase energy expenditure, although this was not directly studied.

One of the mechanisms that links the metabolic syndrome with hepatic steatosis is insulin stimulation of lipogenesis, which can lead to fatty liver and worsening insulin resistance, leading to greater stimulation of lipogenesis Nuclear receptors have the potential to suppress SREBP-1c, which is a pathway that promotes insulin sensitivity. TR isoform agonists have been the primary target for drug development, especially for the treatment of hypercholesterolemia and obesity Table 4.

Animal studies, however, found that long-term use of eprotirome was associated with cartilage breakdown This finding has discouraged development of these agents for broader clinical use despite their effectiveness in direct metabolic actions. The T 4 analog DITPA, originally studied for its property to enhance cardiac function 96 , was found in human trials to have potent actions stimulating metabolism and promoting weight loss The patients treated with DITPA for 6 mo had a reduction in serum total and LDL cholesterol, but also had evidence of increased bone turnover, suggestive of the complications seen with eprotirome.

Although DITPA is a potent agent mediating weight loss, there is concern that at the doses required for the metabolic effects, the skeletal actions may limit its usefulness for metabolic disorders. Thyroid disease has well-documented effects on glucose homeostasis. Thyroid hormone actions in the liver, white adipose tissue, skeletal muscle, and pancreas influence plasma glucose levels, insulin sensitivity, and carbohydrate metabolism.

Reduced activity of mitochondria has been a link between a well-described action of thyroid hormone and a defect in type 2 diabetes It has been previously established that T 3 stimulates gluconeogenesis, especially in the hyperthyroid state, and that hypothyroidism is associated with reduced gluconeogenesis Treatment with T 4 increases alanine transport into hepatocytes, increasing production of metabolic intermediate of the gluconeogenic pathway and ultimately conversion of alanine into glucose Evaluation of T 3 treatment on target genes in the liver reveals that there is an increase in genes regulating glycogenolysis and gluconeogenesis The hepatic insulin resistance was mediated by sympathetic stimulation.

In a follow-up study, administration of T 3 to the hypothalamic paraventricular nucleus, through interaction with the SNS, increases glucose production via sympathetic input to the liver, showing that the T 3 effect was central These animals are more sensitive to insulin and became hypoglycemic after an insulin injection that did not produce hypoglycemia in the wild-type animals.

Several studies have linked thyroid hormone action with pancreatic islet cell development and function. T 3 acts by stimulating the islet transcription factor Mafa. T 3 is required for the transition of islets to glucose-responsive insulin-secreting cells. Inactivation of D2 gene is associated with insulin resistance and diet-induced obesity Thyroid hormone acts to impair glucose-stimulated insulin release, despite increased islet glucose utilization and oxidation.

Hyperthyroidism and high-fat feeding result in significant impairment of islet function In contrast, physiological T 3 treatment prevents streptozocin-induced islet deterioration and maintains islet structure, size, and consistency T 3 induces these anti-apoptotic effects via nongenomic activation of the AKT signaling pathway.

Hepatic glucose output is increased in hyperthyroidism due to increased gluconeogenesis. The rates of insulin-stimulated glucose disposal in peripheral tissues, therefore, must be altered to maintain euglycemia. In the hyperthyroid state, skeletal muscle glucose uptake is increased to overcome a depletion in glycogen stores Similar results were reproduced in Zucker rats, but a notable finding was that T 3 treatment reversed hyperinsulinemia, but not hyperglycemia, in obese animals A study in rats supports a dissociation of thyroid hormone effects on BAT thermogenesis from glucose uptake and control Although thyroid hormone can influence glucose levels, the primary action in the context of this rat diabetes model was on energy expenditure, which did not influence the hyperglycemia.

The interaction of thyroid status and diabetes is complex. Patients with type 1 diabetes have an increase in prevalence rates of autoimmune thyroid disorders compared with the nondiabetic population, especially among women This is thought to be due to similar genetic susceptibility to both autoimmune conditions Studies investigating the interaction of type 2 diabetes and thyroid dysfunction, however, have not shown a consistent association 61 , 99 , Conversely, in severely thyrotoxic patients, the calculated metabolic clearance rate of insulin is markedly higher than control patients, contributing to hyperglycemia in the thyrotoxic state In a recent case report, a patient with severe insulin resistance improved dramatically after suppressive dose levothyroxine for thyroid cancer Imaging of the patient when hypothyroid and then after replacement was restored showed induction of BAT, highlighting the role of TH in insulin sensitivity and energy expenditure.

These genes are induced by physiological doses of T 3 , and pretreatment with a PI3K inhibitor abolishes this effect Systemic administration of T 1 AM rapidly increases endogenous glucose production, glucagon, and corticosterone but does not increase plasma insulin Central administration of T 1 AM resulted in a much more profound effect on endogenous glucose production and hyperglucagonemia and reduced plasma insulin The effects of T 1 AM on glucose and insulin, like the effects of TH, likely vary with the mode and duration of exposure.

Significant progress has been made in understanding TH targets that mediate metabolic regulation. Several themes have emerged which coordinate these signaling pathways, including nutrient feedback at the cellular and central level, nutrient nuclear receptor crosstalk, local ligand activation, and adrenergic stimulation. This has led to mechanistic insights, especially understanding those factors that modulate multiple TH-regulated pathways. A number of these mechanisms are actively being evaluated as therapeutic targets for metabolic diseases.

Although several thyroid hormone analogs have shown significant success in reducing serum LDL cholesterol and producing weight loss, the broad effects of these compounds have limited their clinical application.

TH directly regulates metabolic rate, body weight, and cholesterol metabolism Table 2. TH regulates the expression of target genes directly through TR binding to specific TREs, as well as nongenomic modification of cell signaling.

New evidence highlights the coordinate roles of central and peripheral regulation of TH in modulating metabolic pathways.

TH interacts with the SNS in a synergistic and complementary fashion to maintain homeostasis. In addition, adipokine and neuropeptide regulation of the HPT axis and thermogenesis integrates information on energy availability, storage, and utilization to gauge the regulation of appetite, basal metabolic rate, and body weight. Bile acid stimulation of D2 and local thyroid hormone activation is another unexpected signaling link.

Interference with thyroid hormone signaling is associated with obesity and hepatic steatosis. Finally, emerging evidence identifies a role for TH in glucose metabolism including actions in pancreatic islet development, gluconeogenesis, and insulin signaling. An improved understanding of the mechanism underlying the actions of TH on lipid metabolism and thermogenesis has led to several useful compounds targeting TR for treatment of metabolic disorders 30 , , Table 4.

The thyroid hormone-related thyronamine signaling is a novel pathway to consider for treatment of obesity and metabolic disturbances 88 , The thyronamines are measurable in normal human sera and tissues Acute T 1 AM treatment in animals induces hypothermia and reduces metabolism, similar to torpor in hibernating mammals.

Although the factors that regulate endogenous T 1 AM levels are not known, this is a pathway that could potentially be antagonized to raise metabolic rate. T 1 AM, however, also has the property of rapidly converting an animal from carbohydrate to exclusive fat metabolism, which persists after acute T 1 AM stimulation Selective augmentation of this T 1 AM action is an attractive target for the treatment of metabolic disorders.

Nuclear receptors play a key role in metabolic regulation and are attractive therapeutic targets for metabolic disorders. A significant limitation of their use, however, is unintended metabolic consequences of these agents as well as adverse effects at other sites TR agonists at doses sufficient for favorable metabolic action, such as weight loss and cholesterol lowering, have been associated with adverse action on bone, cartilage, and the heart Ultimately, more selective and specific agents targeting TH signaling pathways, based on improved mechanistic understanding, will be needed to effectively and selectively target metabolic diseases.

No conflicts of interest, financial or otherwise, are declared by the authors. Address for reprint requests and other correspondence: G. Brent, Dept. National Center for Biotechnology Information , U. Physiol Rev. Author information Copyright and License information Disclaimer. Corresponding author. This article has been cited by other articles in PMC. Abstract Thyroid hormone TH is required for normal development as well as regulating metabolism in the adult.

Open in a separate window. Table 1. Sites of thyroid hormone action in metabolic regulation. Table 2. Common themes integrating thyroid hormone metabolic regulation. Thyroid receptor isoforms TH action is exerted primarily via the nuclear TR, a member of the superfamily of hormone-responsive nuclear transcription factors that share a similar structure and mechanism of action 28 , Retinoid X receptor Retinoid X receptor RXR is best characterized as a heterodimer partner that binds with other nuclear receptors to DNA response elements, but it can also be directly stimulated by ligand and regulate gene expression.

Nuclear receptor coregulators Coactivators associate with liganded nuclear receptors and enhance gene transcription Resistance to TH The recognition of TR isoform-specific actions has come from animal models of TR gene mutations and inactivation as well as the phenotype of individuals with TR gene mutations 28 , 29 Table 3.

Table 3. Metabolic manifestations in resistance to thyroid hormone. Role of Deiodinases The intracellular action of TH is regulated by the amount of local T 3 available for receptor binding 90 , Intracellular Transport It had generally been assumed that thyroid hormone, due to its hydrophobicity, enters cells via passive diffusion. Nongenomic Actions TH hormone action is not limited to nuclear receptor mediated T 3 actions that increase or decrease gene transcription, but include nongenomic actions Hypothalamic-Pituitary-Thyroid Axis TH is secreted from the thyroid gland under the regulation of the hypothalamic-pituitary axis Figure 1.

Thyronamines The metabolic effects of TH are also influenced by thyronamines, such as 3-iodothyronamine T 1 AM and fully deiodinated thyronamine T 0 AM , which are decarboxylated and deiodinated analogs of thyroid hormone Facultative Thermogenesis Homeothermic species have developed a nonshivering or facultative thermogenesis to maintain core body temperature after cold exposure and increase energy expenditure after eating.

Skeletal Muscle Skeletal muscle has been recognized as a key TH target for contractile function, regeneration, and transport as well as for metabolism and glucose disposal , Regulation of Body Weight It is well established that thyroid status, either hypothyroidism or hyperthyroidism, is associated with changes in weight and REE.

Regulation of Cholesterol Synthesis TH regulates cholesterol synthesis through multiple mechanisms. Cholesterol Efflux Reverse cholesterol transport is a complex process that results in transfer of cholesterol to the liver for elimination as bile acids or neutral steroids.

Bile Acid Synthesis The conversion of cholesterol to bile acids is required to maintain cholesterol homeostasis. Fatty Acid Metabolism TH stimulates both lipolysis and lipogenesis, although the direct action is lipolysis with lipogenesis thought to be stimulated to restore fat stores TR Isoforms as Therapeutic Targets TR isoform agonists have been the primary target for drug development, especially for the treatment of hypercholesterolemia and obesity Table 4. Table 4. Metabolic properties of natural and synthetic thyroid compounds.

Gluconeogenesis It has been previously established that T 3 stimulates gluconeogenesis, especially in the hyperthyroid state, and that hypothyroidism is associated with reduced gluconeogenesis Insulin Production and Action Several studies have linked thyroid hormone action with pancreatic islet cell development and function.

Thyroid Status and Diabetes The interaction of thyroid status and diabetes is complex. Integrating Mechanisms of Thyroid Hormone Regulation of Metabolism TH directly regulates metabolic rate, body weight, and cholesterol metabolism Table 2.

Therapeutic Targets for Metabolic Disorders An improved understanding of the mechanism underlying the actions of TH on lipid metabolism and thermogenesis has led to several useful compounds targeting TR for treatment of metabolic disorders 30 , , Table 4. Thyroid hormone regulates hepatic expression of fibroblast growth factor 21 in a PPARalpha-dependent manner.

Dietary cholesterol fails to stimulate the human cholesterol 7alpha-hydroxylase gene CYP7A1 in transgenic mice. Thyroid hormone promotes postnatal rat pancreatic beta-cell development and glucose-responsive insulin secretion through MAFA. Resting energy expenditure is sensitive to small dose changes in patients on chronic thyroid hormone replacement.

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This has lead some researchers to believe that there is another cause of the elevation of TSH that is not related to low levels of circulating thyroid hormones. Currently, a popular theory is that insulin resistance leads to changes in the thyroid that can result in changes in the gland and possibly in TSH levels of thyroid hormone levelsvi. Other things being examined are associations with leptin and adiponectin.

There is enough evidence for undiagnosed thyroid disease in obesity, that if you have excess weight or obesity, it is probably a good idea to have your thyroid checked with your annual labs.

This is even truer if you are female or know that you have insulin resistance or diabetes, because of the increased risk. The most common tests used to evaluate the thyroid are:. To learn more about thyroid disease, you can talk to your doctor or visit the following Web sites for more information:. She is the Chief Science Officer for Catalina Lifesciences LLC, a company dedicated to providing the best of nutritional care to weight-loss surgery patients.

Her greatest love is empowering patients to better their own health. High prevalence of previously unknown subclinical hypothyroidism in obese patients referred to a sleep clinic for sleep disordered breathing. Nutr Metab Cardiovasc Dis. Prevalence of subclinical hypothyroidism in a morbidly obese population and improvement after weight loss induced by Roux-en-Y gastric bypass.

Obes Surg. Obesity is associated with increased serum TSH level, independent of thyroid function. Swiss Med Wkly ;— v Marina A. Michalaki, Apostolos G. Vagenakis, Aggeliki S. Leonardou, Marianna N. Argentou, Ioannis G. Habeos, Maria G. A malfunctioning pituitary gland can likewise coax your thyroid gland into gushing out too much thyroid hormone. In some cases, a healthcare provider may prescribe thyroid medication to help rebalance hormone levels in the body.

Remember when we were talking about TSH levels? TSH is a hormone released by the pituitary gland that stimulates the thyroid gland to produce more thyroid hormones.

Related: Hypothyroidism vs. Related: Foods that help thyroid function. For men and non-pregnant women, the recommended daily allowance for iodine is micrograms mcg. For pregnant women, that number rises to mcg per day — and mcg a day for women who are breastfeeding. Of course, if your thyroid hormone level isn't within a normal range and you may have a thyroid dysfunction, consult with your healthcare provider to learn what solution is best for you to help get your hormone levels back in balance in some cases, thyroid hormone replacement may be recommended.

If you do have a thyroid disorder or thyroid condition, your healthcare provider may recommend ongoing thyroid testing to monitor results of your treatment plan. Your thyroid gland is a key part of your metabolic health. But your well-being can slide downhill when your thyroid hormone levels are too high — or too low. Testing your thyroid hormone levels with the Everlywell at-home Thyroid Test is an easy, effective way to check on the status of your thyroid—from the comfort of your home.

And our at-home Thyroid Test is more than just a TSH test: it measures TSH in addition to the thyroid hormones T3 and T4 plus TPOab —giving you a comprehensive, easy way to see if you might have too much or not enough thyroid hormones in your body. Blog Topics. Related: Foods that help thyroid function For men and non-pregnant women, the recommended daily allowance for iodine is micrograms mcg. Conclusion Your thyroid gland is a key part of your metabolic health. Everlywell makes lab testing easy and convenient with at-home collection and digital results in days.