Parathyroid Glands

Parathyroid Glands

Overview and Definition

The parathyroid glands are endocrine glands occurring in all vertebrate species from amphibia upward, usually located close to and behind the thyroid gland. In humans, the parathyroid glands are four pea-sized endocrine glands embedded within the back side of the thyroid; they produce and release parathyroid hormone (PTH). The major function of the parathyroid glands is to maintain the body's calcium and phosphate levels within a very narrow range, so that the nervous and muscular systems can function properly, and they do this by secreting parathyroid hormone (PTH).

Anatomy and Histological Structure

Macroscopic Anatomy and Location

The parathyroid glands are tiny, round structures usually found embedded in the posterior surface of the thyroid gland, separated from the thyroid tissue by a thick connective tissue capsule. Humans usually have four parathyroid glands, each composed of closely packed epithelial cells separated by thin fibrous bands and some fat cells. Each gland weighs about 50 mg (0.002 ounce). Most people have four parathyroid glands, but occasionally there are more in tissues of the neck or chest.

Anatomically, the glands can be divided into two pairs: the superior parathyroid glands, derived embryologically from the fourth pharyngeal pouch, are usually located at the level of the inferior border of the cricoid cartilage. The inferior parathyroid glands are derived embryologically from the third pharyngeal pouch. The parathyroid glands arise in the embryo from the third and fourth pairs of branchial pouches, bilateral grooves resembling gill slits in the neck of the embryo.

Cell Types

The primary functional cells of the parathyroid glands are the chief cells — epithelial cells that produce and secrete parathyroid hormone (PTH), the major hormone involved in the regulation of blood calcium levels. The gland also contains oxyphil cells, but their function is not clear. PTH is exclusively produced and secreted by chief cells located in the parathyroid gland.

Physiological Functions

Parathyroid Hormone (PTH): Structure and Synthesis

Parathyroid hormone (PTH) is a polypeptide containing 84 amino acids that is secreted by the parathyroid glands after cleavage from preproparathyroid hormone (115 amino acids) to proparathyroid hormone (90 amino acids) to the mature hormone. Parathyroid hormone (also known as parathormone) is a small protein that takes part in the control of calcium and phosphate homeostasis, as well as bone physiology. PTH levels can be measured through immunoassays of blood samples, with normal levels ranging from 10 to 65 pg/mL.

Calcium Homeostasis

Calcium homeostasis is a complex process involving four key components: serum calcium, serum phosphate, 1,25-dihydroxyvitamin D-3, and parathyroid hormone (PTH). More than 99% of the calcium in the body is stored in bone as hydroxyapatite, providing both skeletal strength and a reservoir for calcium to be released into the serum. When blood calcium levels drop below a certain point, the calcium-sensing receptors in the parathyroid gland are activated, and the parathyroid glands release PTH into the blood.

The Calcium-Sensing Receptor (CaSR)

The calcium-sensing receptor (CaSR) is a class C G-protein-coupled receptor (GPCR) that plays a fundamental role in extracellular calcium homeostasis by regulating parathyroid hormone (PTH) release. The parathyroid glands express abundant calcium-sensing receptor (CaSR) mRNA and protein; small changes in extracellular Ca²⁺ trigger CaSR-mediated intracellular signaling and PTH secretion, a relationship described by a steep sigmoidal curve. The body controls parathyroid hormone levels by identifying how much calcium is in the blood in a feedback loop: low blood calcium levels trigger PTH release, while high blood calcium levels prevent the glands from releasing PTH.

Actions of PTH on Target Organs

The major target end organs for PTH action are the kidneys, skeletal system, and intestine.

• Bone: PTH increases blood calcium levels by directly stimulating osteoblasts and thereby indirectly stimulating osteoclasts (through RANK/RANKL mechanism) to break down bone and release calcium. Before osteoclast activity, PTH directly stimulates osteoblasts, which increases their expression of RANKL, a receptor activator for nuclear factor kappa-B ligand. PTH also inhibits the secretion of osteoprotegerin — which normally competitively binds RANKL, diminishing the ability to form osteoclasts — thereby allowing osteoclasts to remodel bones by dissolution and degradation of hydroxyapatite and other organic material, releasing calcium into the blood.
• Kidneys: In the kidney, PTH blocks reabsorption of phosphate in the proximal tubule while promoting calcium reabsorption in the ascending loop of Henle, distal tubule, and collecting tubule. PTH also facilitates the synthesis of active vitamin D (calcitriol, or 1,25-dihydroxycholecalciferol) in the kidneys.
• Intestine: PTH acts on the gastrointestinal tract to increase blood calcium by increasing the activity of the enzyme in the intestines that activates vitamin D. The primary action of 1,25-(OH)₂D₃ is to promote gut absorption of calcium by stimulating formation of calcium-binding protein within the intestinal epithelial cells.

Anabolic versus Catabolic Actions on Bone

While PTH stimulates both bone formation and bone resorption, the duration and periodicity of exposure to PTH governs the net effect on bone mass — that is, whether the effect is catabolic or anabolic. Late in the nineteenth century it was theorized that a circulating product produced by the parathyroid glands could negatively impact skeletal homeostasis; a century later, intermittent administration of PTH was approved by the FDA and EMA as the first anabolic agent to treat osteoporosis.

Phosphate Regulation

PTH is the major regulator of serum phosphate concentrations via actions on the kidney. The calcium-sensing receptor (CaSR) is expressed abundantly in parathyroid glands and renal tubules, and it maintains Ca²⁺ homeostasis by modulated suppression of PTH secretion and renal calcium reabsorption in response to increased extracellular calcium. By sensing moderate changes in extracellular phosphate concentration, the CaSR also represents a phosphate sensor in the parathyroid gland, explaining the stimulatory effect of phosphate on PTH secretion.

Fibroblast Growth Factor 23 (FGF23) and the PTH Axis

The calcium and phosphate homeostasis is regulated by a complex interplay between PTH, fibroblast growth factor 23 (FGF23), and calcitriol; experimental studies have demonstrated an inhibitory effect of FGF23 on PTH production and secretion, though the physiological role of this regulation is not well understood. Research using intravenous recombinant FGF23 in rats demonstrated that FGF23 rapidly inhibited PTH secretion through the FGF receptor, with inhibition of that receptor itself significantly increasing PTH levels, indicating that FGF23 exerts a suppressive tonic effect on PTH secretion. FGF23 may also inhibit PTH secretion through an action that requires binding to the FGF receptor and the co-receptor alpha-Klotho.

Calcitonin and Counter-Regulation

PTH works in concert with calcitonin, produced by the thyroid, to maintain calcium homeostasis: PTH acts to increase blood calcium levels, while calcitonin acts to decrease blood calcium levels. When blood calcium levels are high, calcitonin is produced and secreted by the parafollicular cells of the thyroid gland; calcitonin inhibits the activity of osteoclasts, reduces the absorption of dietary calcium in the intestine, and signals the kidneys to reabsorb less calcium, resulting in larger amounts of calcium excreted in the urine. The primary calcium-regulating hormones that control this homeostatic system are PTH and vitamin D, which act at bone, kidney, and gastrointestinal tract to increase serum calcium; calcitonin decreases bone resorption but does not appear to have a major effect on serum calcium under normal circumstances.

Assessment of Parathyroid Health

Laboratory Evaluation

Parathyroid gland dysfunctions are characterized as under-activity or overactivity and are evaluated in the context of serum calcium; whenever a calcium imbalance is suspected or found, the following pertinent labs are initially obtained: PTH, calcium, phosphate, albumin, vitamin D, and magnesium. If blood is found to have high levels of calcium, suppressed levels of PTH (lower than the normal range of 10–65 ng/L) would be expected; if serum PTH is found elevated in the context of hypercalcemia, further investigation of the parathyroid gland is warranted.

Imaging Studies

For suspected parathyroid gland pathology, ultrasound is the first imaging modality utilized due to its efficiency and cost-effectiveness; ultrasound will usually be able to identify the presence of an adenoma as a hypoechoic mass.

A sestamibi scan is a highly sensitive and specific nuclear medicine test used to locate and image an overactive parathyroid gland in a patient with known hyperparathyroidism, and information from the test can help with planning for surgery to remove the overactive gland. By using a gamma camera in nuclear medicine, the radiologist is able to determine if one of the four parathyroid glands is hyperfunctioning; the hyperfunctioning parathyroid gland will take up more of the Tc99m-sestamibi and will show up "brighter" than the other normal parathyroid glands on the gamma camera pictures. Imaging is not as reliable in patients with multiglandular parathyroid disease, and size limitation of the abnormal gland can limit detection by radionuclide scanning.

A bone density study may also be performed, with scans of the hip, lower back, or forearm measuring the amount of calcium in the bones to assess bone health. Other imaging, such as enhanced contrast CT and MRI, also have their place in the clinical investigation of hyperparathyroidism.

Nutrients and Natural Ingredients That Support Normal Parathyroid Function

Vitamin D

Physiological Role

The interplay between vitamin D and parathyroid hormone (PTH) represents one of the most important metabolic mechanisms of regulation of calcium/phosphorus homeostasis. Vitamin D is a fat-soluble secosteroid that plays a central role in calcium homeostasis and bone metabolism through feedback of calcium, phosphate, and PTH; vitamin D deficiency can cause secondary hyperparathyroidism, which must be differentiated from primary hyperparathyroidism (PHPT). Apart from serum calcium, epinephrine, calcitonin, vitamin D, magnesium, and phosphate regulate the synthesis and release of PTH in humans.

Scientific Evidence

Secondary hyperparathyroidism is a major complication that arises as a result of reduced vitamin D levels, both as primary 25-hydroxy-vitamin D (25[OH]D) and/or 1,25-dihydroxyvitamin D (1,25[OH]₂D) reduction. A cross-sectional study published in PMC (2015) found that of 188 participants who were either vitamin D insufficient or deficient, 91 (48.4%) had secondary hyperparathyroidism; those with normal 25-OHD levels had normal PTH levels. Furthermore, all patients with vitamin D deficiency as diagnosed by HPLC-LC.MS had secondary hyperparathyroidism.

Vitamin D repletion is recommended in all forms of PHPT, but the threshold to replace to is controversial; recent studies and meta-analyses suggest that a 25(OH)D threshold level of greater than 30 ng/mL is reasonable to prevent secondary stimulation of PTH secretion and to maintain stable serum and urinary calcium levels.

Evidence strength: The link between vitamin D status and PTH secretion is well established through multiple cross-sectional studies, clinical trials, and mechanistic research. Therapeutic intervention with vitamin D in secondary hyperparathyroidism is supported by substantial clinical evidence, particularly in the setting of chronic kidney disease and populations at risk for vitamin D insufficiency.

Calcium

Physiological Role

Calcium is required for a variety of important physiologic processes, including neuromuscular functioning; thus, blood calcium levels are closely regulated. Dietary calcium intake provides the substrate whose circulating concentration is the principal trigger for PTH secretion. A slight fall in serum calcium is enough to trigger parathormone secretion from the parathyroid cells, and chronically low serum calcium concentrations, which occur as a result of conditions such as vitamin D deficiency and kidney failure, cause abnormal increases in parathormone secretion.

Scientific Evidence

Adequate dietary calcium intake is recognized by authoritative sources as fundamental to normal parathyroid function. In the diagnosis of normocalcemic primary hyperparathyroidism, exclusion of all secondary causes is required, including vitamin D deficiency, renal insufficiency, inadequate calcium intake, hypercalciuria, magnesium deficiency, or medication effects. Hypoparathyroidism treatment primarily consists of correcting calcium, vitamin D, and magnesium deficiencies with supplementation.

Evidence strength: Calcium's role in PTH feedback regulation is very well established mechanistically and through extensive clinical experience. The evidence is rated as strong for its fundamental physiological role; isolated calcium supplementation as a modulator of parathyroid function in otherwise healthy individuals has not been extensively studied in randomized controlled trials, but it forms part of standard management in hypoparathyroidism.

Magnesium

Physiological Role

Magnesium is required for normal parathyroid function, and disordered magnesium levels can exacerbate hypoparathyroidism. One of the most important factors underlying hypocalcemia in hypomagnesemia conditions is the impaired secretion of parathyroid hormone (PTH), referred to as paradoxical hypoparathyroidism.

Scientific Evidence

A classic clinical study published in the Journal of Clinical Endocrinology & Metabolism (Anast et al., 1976) found that the release of parathyroid hormone is impaired in magnesium deficiency and that the level of circulating calcium required for the suppression of parathyroid hormone secretion is lower than that in normal subjects. Intravenous administration of 3 mg/kg of body weight of magnesium led to an abrupt and striking increase in circulating iPTH, with a 2-fold increase in one minute, a 6-fold increase in two minutes, and an 8-fold increase in five minutes.

A subsequent study in the Journal of Clinical Endocrinology & Metabolism (1978) investigating the effect of acute elevation of serum magnesium on PTH in hypomagnesemic patients found that all hypomagnesemic patients had an immediate rise in serum immunoreactive PTH concentration after magnesium administration regardless of the basal PTH concentration. In contrast, normal individuals and patients with primary and secondary hyperparathyroidism responded to magnesium administration with either a decrease or little change in serum PTH concentration.

A case study published in PubMed (2008) documented that magnesium deficiency caused impaired secretion of PTH from the parathyroid and refractoriness of bone and kidney to the hormone, leading to suppression of both bone remodeling and renal vitamin D production. Intravenous administration of magnesium not only improved electrolyte abnormalities but also increased serum levels of intact PTH, bone formation markers, 1,25-dihydroxyvitamin D, and bone resorption markers.

A narrative review published in Kidney Medicine (2025) confirmed that because there is a positive functional correlation and association between serum magnesium and calcium concentrations, clinical hypocalcemia in cases of magnesium deficiency cannot be sufficiently corrected by supplementation with calcium, vitamin D, or both.

An in vitro study in rat parathyroid glands (PubMed, 2013) found that increasing magnesium concentrations from 0.5 to 2 mM produced a left shift of PTH-calcium curves, and with 5 mM magnesium the secretory response was practically abolished; magnesium was able to reduce PTH only if parathyroid glands were exposed to moderately low calcium concentrations. This evidence is preclinical (in vitro) and requires cautious interpretation.

Evidence strength: The role of magnesium in enabling normal PTH secretion is well-documented in clinical and mechanistic studies. Evidence from human clinical studies (including intravenous magnesium repletion trials) confirms that severe hypomagnesemia impairs PTH secretion. This relationship is clinically important and recognized in standard endocrinology guidelines. The in vitro dose-response data add mechanistic detail but do not directly translate to oral supplementation dosing in humans.

Phosphorus / Inorganic Phosphate

Physiological Role

Phosphate levels are normally maintained between 0.8 and 1.4 mM by coordinated regulation of intestinal absorption, renal excretion, and influx/efflux from bone. Elevated dietary phosphate intake can stimulate PTH secretion via the CaSR. Elevated inorganic phosphate levels promote excessive parathyroid hormone secretion, which contributes to the aetiology of secondary hyperparathyroidism.

Evidence strength: The role of dietary phosphate as a regulator of PTH secretion via the CaSR is supported by mechanistic and preclinical evidence as well as observational data in chronic kidney disease populations. Dietary phosphate restriction as a modulator of PTH in non-CKD populations requires further clinical investigation.

Herbs and Natural Ingredients: Traditional Use vs. Scientific Evidence

Important note: Unlike the nutrient co-factors above, no herbs have been rigorously validated in peer-reviewed, controlled clinical trials as specifically supporting or modulating parathyroid gland function. The mentions below reflect traditional or anecdotal use contexts only; the scientific evidence for any direct, specific action on the parathyroid gland from herbs is absent or extremely preliminary.

Vitex agnus-castus (Chaste Tree)

Traditional Use

Chaste tree (Vitex agnus-castus) has been used traditionally to support the parathyroid gland, though it is important to note that this herb can have hormonal effects and interact with medications. This traditional use is derived from Western herbal medicine contexts, where Vitex has been used for endocrine and hormonal concerns more broadly.

Scientific Evidence

No peer-reviewed clinical studies investigating Vitex agnus-castus specifically in relation to parathyroid gland function, PTH levels, or calcium homeostasis could be identified in searches of PubMed or other authoritative databases. Its reported use in this context is traditional and not scientifically validated for parathyroid effects.

Withania somnifera (Ashwagandha)

Traditional Use

Ashwagandha is an adaptogenic herb with a long history of use in Ayurvedic medicine, where it has been employed for endocrine and stress-related conditions broadly. It has been mentioned in integrative health contexts in relation to parathyroid and thyroid gland support. Its Ayurvedic use encompasses general endocrine tonic and adaptogenic applications rather than parathyroid-specific uses.

Scientific Evidence

Preclinical and limited clinical research has examined Withania somnifera for various biological activities including anti-inflammatory and antioxidant effects. No peer-reviewed clinical or experimental studies specifically investigating ashwagandha's effect on PTH, CaSR activity, or parathyroid gland function were identified in authoritative database searches. Claims of its ability to regulate the parathyroid glands in humans are not supported by published clinical evidence.

Glandular Parathyroid Extracts (Glandular Therapy)

Traditional Use

Although parathyroid is not a common ingredient in traditional herbal combinations, it is sometimes paired with other glandular extracts — such as adrenal or thyroid tissues — in multi-glandular supplements formulated to provide comprehensive endocrine support, aiming to balance energy, vitality, and mineral metabolism. The use of animal glandular extracts for health support dates to the late 19th and early 20th centuries in naturopathic and early integrative medicine traditions.

Scientific Evidence

No peer-reviewed clinical trials evaluating the efficacy or safety of oral bovine or porcine parathyroid extracts in humans for normalizing PTH levels or calcium balance were identified in searches of PubMed or equivalent authoritative sources. The scientific basis for oral glandular parathyroid extracts producing specific physiological effects on the parathyroid axis in humans has not been established.

Conditions and Concerns Associated with the Parathyroid Glands

Primary Hyperparathyroidism (PHPT)

Primary hyperparathyroidism (PHPT) is an endocrine disorder defined by autonomous overproduction of parathyroid hormone (PTH), resulting in hypercalcemia and disrupted calcium homeostasis; the most common etiology is a single benign adenoma, while multigland hyperplasia, multiple adenomas, and parathyroid carcinoma are less frequent. PHPT is the leading cause of hypercalcemia in the outpatient setting, predominantly affecting postmenopausal women, and its incidence is rising due to increased routine biochemical screening.

Primary hyperparathyroidism results from overproduction and release of PTH, which can be a result of a parathyroid adenoma, hyperplasia, or carcinoma; in these cases, a single gland or multiple parathyroid glands function above the physiological set point, with elevated PTH and serum calcium and reduced serum phosphate. Since the 1970s, the widespread adoption of automated serum chemistry panels has shifted detection toward asymptomatic disease, with most cases now identified through incidental findings of hypercalcemia; diagnosis currently relies on biochemical confirmation, demonstrated by elevated or inappropriately normal PTH levels in the presence of hypercalcemia.

Normocalcemic Hyperparathyroidism

Normocalcemic hyperparathyroidism presents a unique diagnostic challenge due to its normal serum calcium levels despite elevated parathyroid hormone levels, and it can overlap with primary or secondary hyperparathyroidism, necessitating thorough evaluation to differentiate between these conditions. Longitudinal studies demonstrate that up to 20% of cases progress to classical hypercalcemic PHPT.

Secondary Hyperparathyroidism

Secondary hyperparathyroidism is a physiologic response to a chronic hypocalcemic state; this can be caused by chronic kidney disease (CKD) or vitamin D deficiency. In CKD, the damaged kidneys fail to produce enough 1-alpha-hydroxylase and are therefore unable to convert vitamin D into its active form; additionally, the kidneys are unable to excrete phosphate properly, resulting in higher blood phosphate levels.

Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease, triggered by hyperphosphatemia, hypocalcemia, and low levels of 1,25-dihydroxyvitamin D; SHPT is characterized by parathyroid gland hyperplasia that leads to reduced expression of the vitamin D receptor and CaSR, and chronically elevated PTH secretion.

Tertiary Hyperparathyroidism

Tertiary hyperparathyroidism results from uncorrected long-term hyperparathyroidism, usually seen in end-stage renal disease; chronic low calcium states lead to hyperplasia of the parathyroid glands. The parathyroid glands cannot respond to serum calcium levels and instead act autonomously, producing and secreting PTH, resulting in extremely high PTH levels with elevated calcium and phosphate.

Hypoparathyroidism

Hypoparathyroidism is an uncommon endocrine abnormality in which parathyroid gland dysfunction causes parathyroid hormone deficiency; subsequently, this absence or decreased level of PTH results in hypocalcemia, hyperphosphatemia, and increased neuromuscular irritability.

Though there are multiple causes of hypoparathyroidism, unintended excision or iatrogenic injury during head and neck surgery (e.g., thyroidectomy) is the most common etiology. Other causes of hypoparathyroidism include congenital parathyroid aplasia (as in DiGeorge syndrome), autoimmune destruction, infiltrative processes like hemochromatosis, magnesium deficiency, or genetic mutations in PTH receptors.

Patients typically present with symptoms consistent with hypocalcemia, including myalgias, muscle spasms, twitching, new-onset seizures, and in extreme cases, tetany; symptom severity varies depending on the calcium level and duration of parathyroid dysfunction. Cardiac symptoms associated with conditions such as acute cardiomyopathy and congestive heart failure that result from impaired contractility secondary to hypocalcemia may also occur.

Low blood calcium increases membrane permeability to sodium, resulting in muscle twitching, cramping, spasms, or convulsions; severe deficits can paralyze muscles, including those involved in breathing, and can be fatal.

Pseudohypoparathyroidism

Pseudohypoparathyroidism is a group of disorders characterized by end-organ resistance to the actions of PTH rather than absolute PTH deficiency. A correct diagnosis is very important for this condition, which has a variable presentation and evolving manifestations, and shares many overlapping features with common conditions including hypocalcemia with elevated PTH and hypocalcemia with hyperphosphatemia.

Parathyroid Carcinoma

Parathyroid carcinoma is a less frequent etiology of primary hyperparathyroidism and represents the rarest form of parathyroid pathology. It is associated with markedly elevated PTH and calcium levels and typically presents with more severe symptoms than benign parathyroid disease.

Hypercalcemic Crisis

In patients presenting with acute hypercalcemia, it is important first to correct the electrolyte disturbance as it can be life-threatening; fluid administration is first-line treatment, and the addition of calcium-lowering medications such as diuretics, bisphosphonates, or calcitonin can be used. Once the patient is stabilized, physicians should look for the etiology and treat the underlying disease.

Complications of Untreated Hyperparathyroidism

As blood calcium levels rise, cell membrane permeability to sodium is decreased and the responsiveness of the nervous system is reduced; at the same time, calcium phosphate deposits may collect in the body's tissues and organs (extraosseous calcification), impairing their functioning. Chronic excess PTH leads to skeletal demineralization with increased fracture risk, nephrolithiasis (kidney stones), and progressive renal dysfunction.

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