Corticosteroid-binding globulin (CBG), also known as transcortin, is a key plasma protein that plays a critical role in the transport and regulation of corticosteroids in the bloodstream. Produced primarily by the liver, CBG binds to glucocorticoids such as cortisol, the body’s primary stress hormone. By binding these hormones, CBG regulates their availability and helps control their biological activity. Around 80-90% of circulating cortisol is bound to CBG, ensuring that only a small fraction is free and biologically active. This intricate regulation is crucial for maintaining hormone balance and responding to stress.

CBG is not only responsible for cortisol transport, but it also acts as a reservoir that releases cortisol in response to changing physiological needs. When the body encounters stress, injury, or inflammation, enzymes like neutrophil elastase can cleave CBG, releasing bound cortisol to target tissues. This enables a rapid response to acute stress, increasing the body’s ability to cope with immediate physiological challenges. Without this mechanism, the body would struggle to meet the hormonal demands necessary to maintain homeostasis in stressful situations.

Cortisol / cortisone ratio indicates activity of HSD11B2 activity and assessment of tissue specific concentrations of cortisol, which normally cannot be measured without a biopsy.

Cortisol / cortisone ratio indicates activity of HSD11B2 activity and assessment of tissue specific concentrations of cortisol, which normally cannot be measured without a biopsy.

Cortisol is a steroid hormone synthesized from cholesterol by a multienzyme cascade in the adrenal glands. It is the main glucocorticoid in humans and acts as a gene transcription factor influencing a multitude of cellular responses in virtually all tissues. Cortisol plays a critical role in glucose metabolism, maintenance of vascular tone, immune response regulation, and in the body's response to stress. Its production is under hypothalamic-pituitary feedback control.

Cortisone, a downstream metabolite of cortisol, provides an additional variable to assist in the diagnosis of various adrenal disorders, including abnormalities of 11-beta-hydroxy steroid dehydrogenase (11-beta HSD), the enzyme that converts cortisol to cortisone. Deficiency of 11-beta HSD results in a state of mineralocorticoid excess because cortisol (but not cortisone) acts as a mineralocorticoid receptor agonist. Licorice (active component glycyrrhetinic acid) inhibits 11-beta HSD and excess consumption can result in similar changes.

Cortisol is the main glucocorticoid released from the adrenal gland in response to stress. High levels of cortisol have been reported in cases of Cushing’s disease, malnutrition, early life stress, hypothyroidism, depression, alcoholism, obesity, and critical illness. Additionally, exogenous exposure to glucocorticoids prior to testing may be a source of cortisol elevations.

The Cortisol/day measurement on a HUMAP panel is a crucial indicator of cortisol levels throughout a typical day, reflecting the hormone's diurnal pattern and its overall balance in the body. Cortisol, produced by the adrenal glands, is integral to many bodily functions, such as regulating metabolism, immune response, and the body's stress response. Normally, cortisol levels exhibit a diurnal rhythm: they are highest in the early morning, aiding in waking up and providing energy for the day ahead, and gradually decrease as the day progresses, reaching their lowest levels late in the evening and during early night. This pattern ensures optimal functioning of various physiological processes, including the sleep-wake cycle and blood sugar regulation.

The Cortisol/DHEA-Sulfate (DHEAS) Ratio in the context of the Cortisol Awakening Response (CAR) represents a crucial biomarker in psychoneuroendocrinology, providing valuable insights into the dynamic interplay between the hypothalamic-pituitary-adrenal (HPA) axis and adrenal steroidogenesis under conditions of stress and physiological arousal.

Cortisol, a glucocorticoid hormone, plays a pivotal role in the body's response to stress, influencing various physiological processes, including metabolism, immune function, and circadian rhythm regulation.

DHEAS, an adrenal androgen, serves as a counter-regulatory hormone, often associated with anabolic functions and resilience against stress.

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Salivary cortisone is an inert form of cortisol, as is estrone to estradiol.

Simultaneous testing for cortisol and cortisone assists in diagnosing acquired or inherited abnormalities of 11β-hydroxy steroid dehydrogenase, affecting the cortisol to cortisone ratio.

Deficiency of 11β-HSD results in a state of mineralocorticoid excess because cortisol, not cortisone, acts as a mineralocorticoid receptor agonist.

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Cortisone A (Waking) can help to confirm the marker Cortisol A (Waking).

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Cortisone B (Morning) can help to confirm the marker Cortisol B (Morning).

Cortisone is the inactive form of cortisol. Elevations of cortisone may reflect high cortisol production, excessive 11BHSD2 activity, or insufficient conversion by 11BHSD1.

Cortisone Bedtime as measured on a HUMAP panel is a significant indicator of cortisone levels in the body at bedtime. Cortisone, a metabolite of cortisol, plays a key role in various physiological functions, including the regulation of inflammation, stress response, and metabolic processes. In a healthy individual, cortisone, much like cortisol, follows a diurnal rhythm, with levels typically peaking in the morning and gradually declining throughout the day, reaching their lowest at night. This pattern is critical for maintaining several bodily functions, including the sleep-wake cycle and the body’s ability to recover and rejuvenate during sleep.

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Cortisone C (Afternoon) can help to confirm the marker Cortisol C (Afternoon).

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Cortisone D (Night) can help to confirm the marker Cortisol D (Night).

Cortisone is the inactive form of cortisol. Elevations of cortisone may reflect high cortisol production, excessive 11BHSD2 activity, or insufficient conversion by 11BHSD1.