The Hypothalamic-Pituitary Axis & Peptide Hormones

Your brain runs your endocrine system through a relay station the size of an almond. The hypothalamus, sitting at the base of the brain, produces peptide hormones that travel a few millimeters through a specialized blood supply to reach the pituitary gland. The pituitary, in turn, releases its own hormones into the general circulation, commanding the thyroid, adrenals, gonads, and other target tissues.

This arrangement — the hypothalamic-pituitary axis — is the body's master control system for growth, metabolism, reproduction, and stress response. It works through peptide hormones at every level, and understanding it is fundamental to understanding conditions from hypothyroidism to infertility to Cushing's syndrome.

Architecture of the Axis: How the System Is Built
The HPA Axis: Stress, Cortisol, and CRH
The HPT Axis: Thyroid Function and TRH
The HPG Axis: Reproduction and GnRH
The Growth Hormone Axis: GHRH, Somatostatin, and GH
Feedback Loops: How the System Self-Regulates
Pulsatile Secretion: Why Timing Is Everything
Inhibitory Hypothalamic Peptides
Cross-Talk Between Axes
FAQ
The Bottom Line
References

Architecture of the Axis: How the System Is Built

The Hypothalamus

The hypothalamus occupies just 4 grams of brain tissue, but it integrates signals from nearly every part of the nervous system: circadian clocks, stress inputs, temperature sensors, metabolic status indicators, and reproductive cues. It processes these inputs and converts them into hormonal outputs — small peptide hormones that instruct the pituitary.

The key hypothalamic releasing and inhibiting hormones are all peptides:

Hypothalamic Peptide	Size	Target	Effect on Pituitary
CRH (corticotropin-releasing hormone)	41 amino acids	Corticotrophs	Stimulates ACTH release
TRH (thyrotropin-releasing hormone)	3 amino acids	Thyrotrophs	Stimulates TSH (and prolactin) release
GnRH (gonadotropin-releasing hormone)	10 amino acids	Gonadotrophs	Stimulates LH and FSH release
GHRH (growth hormone-releasing hormone)	44 amino acids	Somatotrophs	Stimulates GH release
Somatostatin	14 amino acids	Somatotrophs, thyrotrophs	Inhibits GH and TSH release
Dopamine	(amine, not a peptide)	Lactotrophs	Inhibits prolactin release

TRH, at just three amino acids (Glu-His-Pro), is among the smallest biologically active peptides in the body. CRH, at 41 amino acids, is among the larger hypothalamic peptides. Despite this size difference, both work through the same fundamental mechanism: they travel through a portal blood system to reach pituitary receptors.

The Hypophyseal Portal System

The hypothalamus and pituitary communicate through a dedicated vascular connection called the hypophyseal portal system. Hypothalamic neurons release their peptides into capillary beds at the median eminence. These capillaries merge into portal veins that descend along the pituitary stalk and feed directly into a second capillary network within the anterior pituitary.

This portal architecture is why hypothalamic peptides can reach the pituitary at high concentrations despite being produced in tiny amounts. The peptides do not dilute into the general circulation — they take a private highway from hypothalamus to pituitary.

The Pituitary Gland

The pituitary gland has two distinct parts with different embryological origins:

Anterior pituitary (adenohypophysis): Contains five cell types that produce six hormones in response to hypothalamic signals:

Corticotrophs: ACTH (39 amino acids, derived from the precursor POMC)
Thyrotrophs: TSH (a glycoprotein hormone)
Gonadotrophs: LH and FSH (glycoprotein hormones)
Somatotrophs: Growth hormone (191 amino acids)
Lactotrophs: Prolactin (199 amino acids)

Posterior pituitary (neurohypophysis): Does not synthesize hormones. Instead, it stores and releases oxytocin and vasopressin, which are produced by hypothalamic neurons and transported down their axons to the posterior pituitary for release.

The HPA Axis: Stress, Cortisol, and CRH

The hypothalamic-pituitary-adrenal (HPA) axis governs the body's stress response and cortisol production.

The Cascade: CRH to ACTH to Cortisol

Stressor detected: Physical, emotional, or metabolic stressors — pain, fear, infection, hypoglycemia, blood loss — activate neural circuits that converge on the hypothalamus.
CRH release: Neurons in the paraventricular nucleus of the hypothalamus secrete CRH (41 amino acids) into the portal circulation. Vasopressin is co-released and synergizes with CRH to amplify the signal.
ACTH secretion: CRH binds to CRH-R1 receptors on pituitary corticotrophs, stimulating the processing of pro-opiomelanocortin (POMC) and the release of ACTH into the bloodstream.
Cortisol production: ACTH travels to the adrenal cortex and binds to melanocortin-2 receptors (MC2R), stimulating the synthesis and secretion of cortisol.
Cortisol effects: Cortisol acts on nearly every tissue. It raises blood glucose through gluconeogenesis, suppresses inflammation, promotes protein catabolism, supports cardiovascular tone, and modulates immune function. It is the body's primary "get through this crisis" hormone.

Negative Feedback

Cortisol completes the loop by feeding back on both the hypothalamus and the pituitary:

At the hypothalamus, cortisol suppresses CRH gene expression
At the pituitary, cortisol suppresses POMC gene expression and ACTH release
This negative feedback keeps cortisol within a normal range and maintains a circadian rhythm — cortisol peaks in the early morning (around 6-8 AM) and reaches its lowest point around midnight

Clinical Disorders: Cushing's and Addison's

When the feedback loop breaks:

Cushing's syndrome results from chronic cortisol excess. A pituitary adenoma secreting excess ACTH (Cushing's disease, ACTH-dependent) or an adrenal tumor autonomously producing cortisol (ACTH-independent) both disrupt the feedback loop. Diagnosis exploits three principles: loss of the cortisol circadian nadir, failure of cortisol to suppress with low-dose dexamethasone, and elevated 24-hour urinary free cortisol.

Addison's disease (primary adrenal insufficiency) results from destruction of the adrenal cortex, most commonly by autoimmune attack. Cortisol is low, but ACTH is elevated because the negative feedback brake has been released. The elevated ACTH (and related POMC-derived peptides like alpha-MSH) explains the characteristic skin hyperpigmentation of Addison's disease — alpha-MSH stimulates melanocytes.

Secondary adrenal insufficiency occurs when the pituitary fails to produce adequate ACTH (from pituitary damage or prolonged exogenous corticosteroid use that suppresses the HPA axis). Both cortisol and ACTH are low. No hyperpigmentation occurs because ACTH is not elevated.

Condition	Cortisol	ACTH	Mechanism
Normal	Normal range	Normal range	Intact feedback
Cushing's disease	High	High	Pituitary adenoma overproducing ACTH
Adrenal Cushing's	High	Low	Adrenal tumor; feedback suppresses ACTH
Addison's disease	Low	High	Adrenal destruction; no feedback
Secondary insufficiency	Low	Low	Pituitary/hypothalamic failure

The HPT Axis: Thyroid Function and TRH

The hypothalamic-pituitary-thyroid (HPT) axis regulates metabolic rate, thermogenesis, growth, and neurodevelopment.

The Cascade: TRH to TSH to T3/T4

TRH release: The hypothalamus secretes TRH, the tripeptide Glu-His-Pro, into the portal system.
TSH secretion: TRH binds to TRH receptors on pituitary thyrotrophs, stimulating TSH (thyroid-stimulating hormone) production and release. TRH also stimulates prolactin release — which is why hypothyroidism (with elevated TRH) can cause galactorrhea.
T4 and T3 production: TSH acts on the thyroid gland to stimulate all steps of thyroid hormone synthesis: iodine uptake, thyroglobulin synthesis, iodination, coupling, and hormone release. The thyroid produces primarily T4 (thyroxine, roughly 80% of output) with a smaller amount of T3 (triiodothyronine).
Peripheral conversion: T4 is the circulating reservoir. It is converted to the active hormone T3 in peripheral tissues (especially liver and kidney) by type 1 and type 2 deiodinases (D1 and D2). Roughly 80% of circulating T3 comes from peripheral T4-to-T3 conversion rather than direct thyroid secretion.
Negative feedback: T3 binds to nuclear thyroid hormone receptors (primarily TRbeta2) in pituitary thyrotrophs and hypothalamic TRH neurons. This suppresses both TSH and TRH production, completing the loop.

The Role of Deiodinases

Deiodinase enzymes act as local amplifiers and silencers of thyroid hormone signaling:

D2 converts T4 to active T3, amplifying the signal. It is expressed in the brain, pituitary, brown adipose tissue, and thyroid.
D3 converts T4 to inactive reverse T3 (rT3), dampening the signal. It is highly expressed in the placenta (protecting the fetus from excess thyroid hormone) and in the brain.
D1 performs both conversions and is the primary source of circulating T3.

In the hypothalamus, D2 is expressed in specialized cells called tanycytes that line the third ventricle. Tanycytes convert T4 to T3, which then diffuses to TRH neurons in the paraventricular nucleus. This local conversion means that hypothalamic feedback depends primarily on circulating T4 levels, even though T3 is the active hormone at the receptor.

Clinical Disorders: Hypo- and Hyperthyroidism

Primary hypothyroidism (e.g., Hashimoto's thyroiditis): Low T4/T3, high TSH. The failing thyroid cannot produce enough hormone, so the pituitary increases TSH in an attempt to compensate. This is the most common thyroid disorder.

Secondary hypothyroidism (pituitary failure): Low T4/T3, low or inappropriately normal TSH. The pituitary is not sending adequate stimulation to a potentially normal thyroid.

Tertiary hypothyroidism (hypothalamic failure): Same biochemical picture as secondary, but caused by insufficient TRH. Seen in hypothalamic damage or euthyroid sick syndrome.

Graves' disease (autoimmune hyperthyroidism): Antibodies mimic TSH and continuously stimulate the thyroid. T4/T3 are elevated; TSH is suppressed by negative feedback.

The HPT axis feedback loop is so tightly regulated that morning TSH concentrations remain remarkably stable from day to day and year to year in healthy individuals. Clinicians use TSH as the single most sensitive marker for thyroid dysfunction — even small changes in free T4 produce amplified changes in TSH.

The HPG Axis: Reproduction and GnRH

The hypothalamic-pituitary-gonadal (HPG) axis controls reproductive function in both sexes.

Pulsatile GnRH: Why Rhythm Matters

GnRH is a 10-amino-acid peptide whose secretion pattern is everything. GnRH must be released in pulses — and the frequency of those pulses determines what happens downstream.

Fast pulses (greater than 1 pulse per hour): Favor LH secretion
Slow pulses (less than 1 pulse every 2-3 hours): Favor FSH secretion

Here is the counterintuitive part: continuous GnRH exposure does not continuously stimulate the pituitary. Instead, it causes GnRH receptor downregulation (desensitization) and paradoxically suppresses LH and FSH production. This paradox is the basis for an entire class of drugs.

At the onset of puberty, the GnRH pulse generator activates, triggering the cascade of sexual development. GnRH secretion is modulated by sex steroid feedback throughout reproductive life and diminishes with menopause and andropause.

Kisspeptin: The Upstream Regulator

GnRH neurons themselves do not have estrogen receptors (ERalpha) or androgen receptors. So how does the system receive sex steroid feedback?

The answer was discovered in the early 2000s: kisspeptin. Kisspeptin neurons in the hypothalamus express sex steroid receptors and project to GnRH neurons. They are the relay between circulating sex steroids and GnRH output.

Two populations of kisspeptin neurons play distinct roles:

Arcuate nucleus kisspeptin neurons: Mediate negative feedback. Rising estrogen or testosterone suppresses these neurons, which reduces GnRH pulse frequency.
AVPV/PeN kisspeptin neurons (in females): Mediate positive feedback. High, sustained estrogen levels (as in the late follicular phase) activate these neurons, triggering the GnRH and LH surges that cause ovulation.

RFRP-3 (RFamide-related peptide-3), the mammalian equivalent of gonadotropin-inhibiting hormone, provides an additional inhibitory input. RFRP-3 neurons in the dorsomedial hypothalamus can suppress both GnRH neurons and kisspeptin neurons, offering a mechanism by which stress can inhibit reproductive function.

Clinical Applications: From Fertility Treatment to Cancer Therapy

Pulsatile GnRH administration can restore fertility in women with hypothalamic amenorrhea by mimicking the natural pulse pattern. A small pump delivers GnRH subcutaneously every 60-90 minutes.

GnRH agonists (leuprolide, goserelin, nafarelin) given continuously cause initial stimulation ("flare") followed by receptor desensitization and profound suppression of LH, FSH, and sex steroids. Clinical uses include:

Prostate cancer (medical castration to reduce testosterone that fuels tumor growth)
Endometriosis and uterine fibroids (reducing estrogen-driven tissue growth)
Central precocious puberty (suppressing premature sexual development)
Fertility treatments (controlled ovarian suppression before stimulation)

GnRH antagonists (cetrorelix, ganirelix, degarelix) block the receptor without the initial flare, producing immediate suppression. Degarelix is used in prostate cancer when the flare effect of agonists is undesirable.

The Growth Hormone Axis: GHRH, Somatostatin, and GH

Growth hormone (GH) secretion is controlled by a dual hypothalamic input system — one stimulatory, one inhibitory.

GHRH and Somatostatin: Gas Pedal and Brake

GHRH (44 amino acids) from the arcuate nucleus stimulates GH release from pituitary somatotrophs by binding to the GHRH receptor (a Class B GPCR). The signal is transduced through the Gs/cAMP/PKA pathway.

Somatostatin (14 amino acids) from the periventricular nucleus inhibits GH release by binding to somatostatin receptors (SST1-5, Class A GPCRs coupled to Gi). Somatostatin also inhibits TSH release and suppresses numerous gastrointestinal hormones — it is the endocrine system's broad-spectrum brake.

The push-pull between GHRH and somatostatin creates GH's characteristic pulsatile secretion pattern. GH is released in bursts, with the largest pulse occurring during deep sleep. Between pulses, somatostatin suppresses GH to near-undetectable levels. This pulsatility is physiologically important — continuous GH exposure is less effective at promoting growth than pulsatile exposure.

Feedback regulation: GH acts on the liver to produce insulin-like growth factor 1 (IGF-1). IGF-1 feeds back to both the hypothalamus (stimulating somatostatin release) and the pituitary (directly inhibiting GH secretion). GH itself also feeds back at the hypothalamic level.

Synthetic GHRH analogs like CJC-1295 are designed to stimulate this axis with modifications that extend the peptide's half-life.

Ghrelin: The Third Input

Ghrelin, a 28-amino-acid peptide produced primarily by the stomach, binds to the growth hormone secretagogue receptor (GHS-R1a) on pituitary somatotrophs and potently stimulates GH release through a pathway independent of GHRH. Ipamorelin is a synthetic growth hormone-releasing peptide (GHRP) that activates this same receptor.

The GH axis therefore has three hypothalamic/peripheral inputs: GHRH (stimulatory), somatostatin (inhibitory), and ghrelin (stimulatory via a separate receptor).

The Somatopause and Therapeutic Targeting

GH secretion declines roughly 14% per decade after age 30 — a process called the somatopause. By age 60, many adults produce less than half the GH they did at 25. IGF-1 levels decline in parallel.

This natural decline has motivated research into:

GHRH analogs (CJC-1295) to stimulate the pituitary's own GH production
Growth hormone secretagogues (ipamorelin) that work through the ghrelin receptor
Combinations of GHRH analogs and GHRPs to exploit synergistic stimulation

The clinical use of exogenous GH itself (recombinant human GH) is FDA-approved for GH-deficient children and adults but remains controversial for "anti-aging" purposes.

Feedback Loops: How the System Self-Regulates

Every hypothalamic-pituitary axis operates through negative feedback loops, and understanding the loop structure is the key to understanding endocrine pathology.

The basic pattern is a three-tier cascade:

Tier 1 (Hypothalamus) → releasing hormone → Tier 2 (Pituitary) → tropic hormone → Tier 3 (Target gland) → end hormone

The end hormone (cortisol, T3/T4, estrogen/testosterone, IGF-1) feeds back to suppress Tier 1 and Tier 2. This negative feedback maintains homeostasis.

Long-loop feedback: End hormones act on the hypothalamus and pituitary (e.g., cortisol suppressing CRH and ACTH).

Short-loop feedback: Pituitary hormones act on the hypothalamus (e.g., GH suppressing GHRH release).

Ultra-short-loop feedback: Hypothalamic hormones inhibit their own release (e.g., GnRH may inhibit its own neurons).

When the system breaks:

Primary gland failure (Tier 3 damage): End hormone drops, Tier 1 and 2 hormones rise (loss of feedback inhibition). Example: Hashimoto's thyroiditis (low T4, high TSH).
Secondary failure (Tier 2 damage): Tropic hormone drops, end hormone drops. Example: pituitary adenoma damaging gonadotrophs (low LH/FSH, low testosterone).
Tertiary failure (Tier 1 damage): Releasing hormone drops, tropic hormone drops, end hormone drops. Example: hypothalamic damage after radiation.

The diagnostic approach is straightforward: measure Tier 2 and Tier 3 hormones simultaneously. Their relative levels tell you which tier is broken.

Pulsatile Secretion: Why Timing Is Everything

Hypothalamic peptides are not released continuously. They are secreted in pulses, and the pulse pattern carries biological information.

GnRH pulse frequency determines the ratio of LH to FSH secretion. Fast pulses favor LH; slow pulses favor FSH. The menstrual cycle is orchestrated by systematic changes in GnRH pulse frequency.

GHRH and somatostatin alternate in a see-saw pattern that creates GH pulses. During sleep, somatostatin tone decreases and GHRH secretion increases, producing the nocturnal GH surge.

CRH secretion follows a circadian pattern superimposed with stress-responsive bursts. The result is the cortisol circadian rhythm with its early-morning peak.

TRH secretion shows circadian variation (TSH peaks at night) and is modulated by cold exposure, fasting, and illness.

This pulsatility has a direct clinical implication: drugs that provide continuous stimulation of these receptors produce different effects than pulsatile stimulation. Continuous GnRH suppresses reproduction; pulsatile GnRH supports it. The receptor cannot distinguish between "too much signal" and "no signal" if the stimulus never lets up — desensitization turns constant stimulation into functional blockade.

Inhibitory Hypothalamic Peptides

Not all hypothalamic peptides are releasing hormones. Two are primarily inhibitory:

Somatostatin (also called somatotropin release-inhibiting factor, SRIF) suppresses GH and TSH from the pituitary and suppresses insulin, glucagon, gastrin, secretin, and many other gastrointestinal hormones. Octreotide and lanreotide are synthetic somatostatin analogs used to treat acromegaly (GH excess) and neuroendocrine tumors.

Dopamine (technically a catecholamine, not a peptide) is the primary inhibitor of prolactin secretion. Prolactin is unique among pituitary hormones because its default state is "on" — without dopamine inhibition, prolactin is continuously secreted. This is why pituitary stalk damage (which interrupts dopamine delivery) causes hyperprolactinemia, not prolactin deficiency.

RFRP-3 (discussed above) is an inhibitory neuropeptide that suppresses the HPG axis.

Cross-Talk Between Axes

The hypothalamic-pituitary axes do not operate in isolation. They interact, sometimes cooperatively, sometimes antagonistically.

Stress suppresses reproduction: CRH and cortisol inhibit GnRH secretion, which is why chronic stress, excessive exercise, and severe caloric restriction can cause amenorrhea and reduced fertility. This makes evolutionary sense — reproduction is not prioritized during survival threats.

Thyroid hormones modulate growth: Adequate thyroid hormone is required for normal GH action. Hypothyroid children have impaired growth despite normal GH levels because T3 is needed for GH receptor expression and IGF-1 production.

TRH stimulates prolactin: The TSH-stimulating effect of TRH extends to prolactin release. In severe hypothyroidism, markedly elevated TRH can cause hyperprolactinemia and even galactorrhea.

Cortisol suppresses growth: Chronic cortisol excess (Cushing's syndrome) suppresses the GH axis and inhibits growth in children. It also reduces bone formation, contributing to osteoporosis.

Illness disrupts multiple axes: Critical illness typically activates the HPA axis (stress cortisol) while suppressing the HPG axis (reduced testosterone) and the HPT axis (euthyroid sick syndrome with low T3). This coordinated response redirects metabolic resources toward survival, but prolonged critical illness can cause significant endocrine dysfunction.

FAQ

What are the main hypothalamic releasing hormones? The four primary peptide releasing hormones are CRH (41 amino acids, stimulates ACTH), TRH (3 amino acids, stimulates TSH), GnRH (10 amino acids, stimulates LH/FSH), and GHRH (44 amino acids, stimulates GH). Somatostatin and dopamine are the main inhibitory signals. All reach the anterior pituitary through the hypophyseal portal system.

Why does continuous GnRH suppress the reproductive axis instead of stimulating it? GnRH receptors require pulsatile stimulation to maintain their expression and signaling capacity. Continuous GnRH exposure causes receptor phosphorylation, internalization, and downregulation — the cell pulls the receptors off its surface because the signal never stops. The result is functional blockade of LH and FSH secretion, even though GnRH is present in abundance.

What is the difference between Cushing's disease and Cushing's syndrome? Cushing's syndrome is the umbrella term for any condition causing chronic cortisol excess. Cushing's disease is the specific subset caused by a pituitary adenoma that overproduces ACTH. Other causes of Cushing's syndrome include adrenal tumors (ACTH-independent cortisol production), ectopic ACTH-secreting tumors (usually lung), and prolonged exogenous corticosteroid use (the most common cause overall).

How do doctors test the HPA axis? Several dynamic tests are used. The low-dose dexamethasone suppression test checks whether exogenous glucocorticoid properly suppresses ACTH and cortisol (it should in healthy individuals, but not in Cushing's). The ACTH stimulation test (Synacthen test) checks whether the adrenals can respond to ACTH (they cannot in Addison's disease). 24-hour urinary free cortisol and late-night salivary cortisol screen for cortisol excess.

Can the hypothalamic-pituitary axis recover after suppression? Yes, in many cases. HPA axis suppression from prolonged corticosteroid use typically recovers gradually over weeks to months after steroids are tapered — which is why abrupt steroid discontinuation is dangerous (risk of adrenal crisis). HPG axis recovery after discontinuation of GnRH analogs also occurs, usually within 3-6 months. However, recovery depends on the duration and cause of suppression, and permanent damage from surgery, radiation, or autoimmune destruction may be irreversible.

The Bottom Line

The hypothalamic-pituitary axis is a cascade of peptide signals — small molecules released in precise pulses that command some of the body's most important physiological processes. CRH controls cortisol and the stress response. TRH controls thyroid function and metabolic rate. GnRH controls reproduction. GHRH and somatostatin balance growth hormone output.

Each axis follows the same three-tier architecture: hypothalamic releasing peptide, pituitary tropic hormone, target-gland end hormone, with negative feedback from the end hormone completing the loop. When the loop works, homeostasis is maintained. When it breaks — at any of the three tiers — recognizable clinical syndromes emerge.

The therapeutic implications span endocrinology: GnRH analogs for prostate cancer and fertility, GHRH analogs and secretagogues for growth hormone optimization, somatostatin analogs for acromegaly, and CRH testing for adrenal disorders. These drugs work because they exploit the architecture of peptide signaling at the hypothalamic-pituitary interface.

For deeper dives into individual peptides mentioned in this article, see our profiles on CJC-1295 (GHRH analog), ipamorelin (GHS-R agonist), oxytocin, and semaglutide (GLP-1R agonist). For the basics of peptide biology, start with our complete beginner's guide.

References

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