on July 19, 2026
What is the thyroid and what is it used for?
The thyroid is a butterfly-shaped endocrine gland located in the anterior region of the neck, playing a primary role in regulating the basal metabolism and energy homeostasis of the entire body. Its follicular cells synthesize and secrete thyroid hormones: thyroxine (T4) and triiodothyronine (T3). These lipid hormones act by binding to specific nuclear receptors (TRalpha and TRbeta), modulating gene transcription and directly influencing protein, carbohydrate, and lipid metabolism, as well as the development of the nervous system and cardiovascular activity.
In addition to the follicular function, the thyroid houses parafollicular cells (or C cells), responsible for the production of calcitonin. This peptide hormone works in close synergy with parathyroid hormone (PTH) — secreted by the parathyroid glands — and with vitamin D to regulate calcemia, promoting the fixation of calcium in the bone matrix and countering osteoclastic resorption. Timely diagnosis of thyroid alterations allows for the establishment of effective therapeutic protocols, preventing severe systemic complications affecting the cardiovascular and metabolic systems.
Are thyroid disorders rare or common?
Thyroid disorders represent one of the most widespread classes of pathologies in the field of endocrinology, ranking just after diabetes mellitus in terms of prevalence. It is estimated that they affect approximately 500,000 people in Italy and over 200 million worldwide. These conditions can result from intrinsic alterations in glandular function (hypo- or hyperthyroidism), inflammatory processes, or surgical removal of the organ.
Hypothyroidism, even in its subclinical forms, affects almost 5% of the general population, with an epidemiological peak reaching 17% in women and 8% in men over 60 years of age. The leading etiological cause in industrialized countries is Hashimoto's chronic thyroiditis, an autoimmune disease characterized by a strong genetic predisposition. Hyperthyroidism shows a prevalence of 2-3% (up to 4-6% in mild forms) and exhibits a clear predilection for the female sex (with a ratio of 10:1 compared to men), manifesting predominantly in the age group between 20 and 40 years, as in the case of Graves' disease. Both dysfunctional conditions reflect on the central and autonomic nervous systems, inducing manifestations overlapping with anxiety disorders, chronic insomnia, and menstrual cycle alterations. Thanks to mass iodine prophylaxis through the use of iodized salt, endemic goiter diseases related to nutritional iodine deficiency are now drastically reduced nationwide.
How are thyroid disorders diagnosed?
The assessment of thyroid function is based on the study of the dynamics of the hypothalamus-pituitary-thyroid axis (HPT axis). The secretion of T3 and T4 is regulated by thyroid-stimulating hormone (TSH) secreted by the anterior pituitary, which is in turn modulated by the hypothalamic releasing factor TRH through a refined negative feedback mechanism (feedback).
The initial diagnostic pathway includes the reflex blood test for TSH and free fractions of thyroid hormones (fT3 and fT4), which reflect the biologically active portion in circulation. At the instrumental level, high-resolution thyroid ultrasound represents the examination of choice for assessing the volume of the gland, the echostructure of the parenchyma, and the presence of nodular formations. In cases where an autoimmune origin is suspected, the diagnostic panel is completed with the determination of anti-thyroperoxidase (anti-TPO) and anti-thyroglobulin (anti-TG) antibodies, as well as TSH receptor antibodies (TRAb), pathognomonic of Graves' disease.
What is hypothyroidism?
Hypothyroidism is a clinical syndrome characterized by insufficient production or peripheral action of thyroid hormones, which causes a generalized slowing down of all metabolic processes in the body. From an etiopathogenetic point of view, it is distinguished in:
· Primary hypothyroidism: caused by an intrinsic dysfunction of the gland itself (e.g., autoimmune destruction, outcomes of thyroidectomy or radioiodine therapy, chronic iodine deficiency or excess).
· Secondary/tertiary hypothyroidism (central): resulting from a secretion deficit of TSH by the pituitary or TRH by the hypothalamus (e.g., pituitary adenomas, trauma, vascular insults).
The cardinal symptoms include severe asthenia, unexplained weight gain, cold intolerance, bradycardia, hypercholesterolemia, stubborn constipation, and cognitive slowing (brain fog). If the pathology is not treated appropriately, it can progress toward severe clinical conditions up to a myxedematous coma, a medical emergency with high mortality.
Is hypothyroidism curable?
The therapeutic management of hypothyroidism is based on the restoration of clinical and biochemical euthyroidism through replacement pharmacological therapy, which in most cases must be continued for life. The therapeutic gold standard is represented by the oral administration of levothyroxine sodium (L-T4).
The clinical strategy involves starting treatment with low doses, especially in elderly or cardiac patients, followed by a progressive dose increase (titration) guided by serial TSH monitoring (performed at intervals of 6-8 weeks from each variation). A critical aspect is related to the intestinal absorption of levothyroxine, which occurs mainly at the gastric and duodenal level and requires an acidic environment. Nutritional and pharmacological factors can significantly interfere with the bioavailability of the active ingredient; it is necessary to separate the intake of L-T4 from iron supplements, calcium carbonate, aluminum hydroxide, or cholestyramine by at least 4 hours. Even a high and concomitant consumption of soy-based products (rich in isoflavones) can reduce its enteric absorption, requiring careful TSH monitoring.
What is hyperthyroidism?
Hyperthyroidism is a clinical condition characterized by a prolonged and increased synthesis and secretion of thyroid hormones by the gland, with consequent thyrotoxicosis and a global acceleration of the basal metabolism. The most frequent cause in young women is Graves' disease, an autoimmune disease in which circulating autoantibodies (TRAb) bind to the TSH receptor, constitutively activating it. This causes diffuse goiter and, frequently, a specific orbitopathy (Basedowian ophthalmopathy) characterized by exophthalmos (bulging eyes), periorbital edema, burning, diplopia, and photophobia.
Other common causes include toxic multinodular goiter and Plummer's toxic adenoma, in which one or more nodules acquire functional autonomy independent of pituitary control. Systemic symptoms include tachycardia, palpitations, weight loss despite increased appetite, fine tremors in the extremities, heat intolerance, hyperkinesia, and emotional lability. Uncontrolled hyperthyroidism exposes the patient to severe complications, such as atrial fibrillation, accelerated osteoporosis, and thyroid storm.
What is the therapy for hyperthyroidism?
The treatment of hyperthyroidism is multifactorial and is personalized based on the etiology, the patient's age, and the severity of the clinical picture. The main therapeutic options are three:
1. Medical therapy with antithyroid drugs: uses thionamides, mainly methimazole (in Europe) and propylthiouracil. These drugs inhibit the thyroperoxidase enzyme (TPO), blocking the organification of iodide and the coupling of iodotyrosines. They require careful specialist monitoring due to the risk of rare but severe adverse effects, such as agranulocytosis and hepatotoxicity.
2. Radioiodine therapy (131I): radioactive iodine is administered orally, selectively taken up by the hyperactive follicular cells, and causes their progressive destruction through local beta radiation. The dosage must be carefully calculated to avoid inducing permanent iatrogenic hypothyroidism.
3. Surgical therapy (Total or Subtotal Thyroidectomy): indicated in cases of large goiters with compressive symptoms, suspicion of malignancy, or failure of other therapies. The surgery carries the risk of recurrent laryngeal nerve injury (resulting in dysphonia) and iatrogenic hypoparathyroidism due to the removal or devascularization of the parathyroids. Total removal entails the immediate initiation of chronic replacement therapy with L-T4.
What is meant by thyroid nodules?
Thyroid nodules are circumscribed structural lesions of the glandular parenchyma, extremely common in the general population. Ultrasound examinations document the presence of nodularity (often non-palpable and sub-centimetric) in between 50% and 60% of healthy subjects, with a clear prevalence in the female sex. About 80% of these formations show characteristics of stability over time (e.g., colloid nodules, cysts), 16.5% show an indeterminate cytological profile requiring further diagnostic investigations, while only 3.5% are an expression of a malignant neoplasm (papillary, follicular, medullary, or anaplastic carcinoma). It should be emphasized that the finding of a nodule in the male sex or in childhood statistically correlates with a higher relative risk of malignancy.
Clinical management is guided by ultrasound risk stratification (EU-TIRADS systems) and cytological examination via fine-needle aspiration (FNAC) for suspicious or lesions larger than one centimeter. Non-secreting benign nodules require exclusively annual clinical and ultrasound follow-up. Surgical removal becomes mandatory in cases of confirmed or suspected malignancy, or in the presence of large benign nodules that exert a mass effect on contiguous structures, causing dysphagia (difficulty swallowing) or dyspnea (difficulty breathing).
What is thyroiditis?
The term thyroiditis defines a heterogeneous group of inflammatory pathologies affecting the thyroid gland, characterized by different clinical courses and a potential transient or permanent alteration of circulating hormone levels. The main forms include:
· Chronic autoimmune thyroiditis (Hashimoto's): characterized by chronic lymphocytic infiltration mediated by T helper lymphocytes and the presence of anti-TPO and anti-TG antibodies. It leads to the progressive destruction of the follicular parenchyma and permanent hypothyroidism. The cornerstone therapy is exclusively replacement with levothyroxine.
· De Quervain's subacute thyroiditis: granulomatous inflammation with a likely viral etiology, preceded by upper respiratory tract infections. It manifests with severe anterior neck pain radiating to the mandibular angle, fever, and a transient phase of release thyrotoxicosis (destruction-induced), followed by hypothyroidism and subsequent restoration of euthyroidism. It is treated with NSAIDs or corticosteroids to control pain and inflammation.
· Infectious acute thyroiditis: of bacterial origin, extremely rare and usually limited to immunocompromised patients or those with anatomical abnormalities (e.g., pyriform sinus fistula). It requires targeted antibiotic therapy and, if necessary, surgical drainage of abscesses.
There are also drug-induced iatrogenic thyroiditis caused by drugs such as amiodarone (an iodinated antiarrhythmic), lithium, interferon-alpha, and modern immune checkpoint inhibitors used in oncology, which require close monitoring of thyroid function.
Are thyroid problems risky during pregnancy?
Thyroid homeostasis is an essential biological requirement for the proper maintenance of pregnancy and fetal neuropsychological development. During the first trimester of pregnancy, the fetus does not have a functioning thyroid gland and depends entirely on the transplacental supply of maternal thyroid hormones. Gestational physiology itself profoundly alters maternal thyroid function: the rise in human chorionic gonadotropin (hCG), which has partial structural homology with TSH, exerts a cross-reactive stimulus on the thyroid, leading to a physiological reduction in TSH during the first few months.
Uncontrolled thyroid conditions expose both the mother and the fetus to severe obstetric risks. Untreated or undertreated maternal hypothyroidism significantly increases the incidence of first-trimester spontaneous abortion, placental abruption, preeclampsia, and preterm birth, and may impair the intellectual and cognitive development of the newborn (lower IQ, neuro-motor delay). Uncontrolled gestational hyperthyroidism can lead to intrauterine growth restriction (IUGR), low birth weight, fetal tachycardia, and maternal heart failure. Therefore, international guidelines recommend screening thyroid function pre-conceptionally or during the first few weeks of pregnancy, with regular monitoring (every 4–6 weeks) to adjust the medication dosage promptly.
How should patients manage total thyroidectomy and replacement hormone therapy?
Total surgical removal of the thyroid gland results in permanent iatrogenic hypothyroidism, requiring chronic levothyroxine (L-T4) supplementation to mimic endogenous production. However, a significant percentage of thyroidectomized patients, despite achieving perfect biochemical compensation (TSH, fT3, and fT4 levels within the normal range), continue to experience symptoms typical of hypothyroidism, such as chronic fatigue, difficulty losing weight, mood changes, water retention, and intestinal dysbiosis. This phenomenon is often linked to the absence of physiological organ conversion and reduced peripheral deiodinase efficiency (the enzymes responsible for converting T4 into the active metabolite T3), as well as a low-grade inflammatory state induced by the loss of glandular homeostasis. In this context, supplementation with targeted functional nutrition and phytotherapeutic protocols represents a fundamental clinical tool for optimizing the effectiveness of pharmacological therapy and restoring systemic well-being.
PLEASE NOTE: The information in this article is for informational and educational purposes only and does not in any way constitute medical or specialist advice. The published content is not intended to and should not replace direct communication with healthcare professionals or any medical advice, diagnosis, or therapeutic prescriptions. Any changes to diet or lifestyle, or the introduction of dietary supplements and phytotherapeutic preparations, particularly in patients who have undergone thyroidectomy and are on levothyroxine therapy, must be thoroughly discussed with and approved by the endocrinologist or treating physician to avoid drug interactions and alterations in therapeutic compensation.
Bibliographic References
· WHO (2009). WHO Monographs on Selected Medicinal Plants, Vol. 4. World Health Organization. (International guidelines on the standardization and safety of phytotherapeutics).
· Jonklaas, J., Bianco, A. C., Cappola, A. R., et al. (2014). Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid, 24(12), 1670–1751. (Clinical guidelines for the management of levothyroxine and its interactions).
· Bianco, A. C., & da Conceição, R. R. (2018). The deiodinase system and peripheral control of thyroid hormone activation. European Thyroid Journal, 7(Suppl. 1), 14–22. (Study on the cellular biological mechanisms of deiodinases and the role of selenium).
