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cortisol, cortisol levels
Cortisol is a steroid hormone, in the glucocorticoid class of hormones When used as a medication, it is known as hydrocortisone

It is produced in humans by the zona fasciculata of the adrenal cortex within the adrenal gland1 It is released in response to stress and low blood-glucose concentration It functions to increase blood sugar through gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbohydrates2 It also decreases bone formation3


  • 1 Health effects
    • 11 Metabolic response
    • 12 Immune response
  • 2 Other effects
    • 21 Metabolism
      • 211 Glucose
      • 212 Bone and collagen
      • 213 Amino acid
    • 22 Wound healing
    • 23 Electrolyte balance
      • 231 Sodium
      • 232 Potassium
    • 24 Stomach and kidneys
    • 25 Memory
    • 26 Sleep, stress, and mood
    • 27 Effects during pregnancy
  • 3 Synthesis and release
    • 31 Normal levels
    • 32 Disorders of cortisol production
  • 4 Regulation
    • 41 Factors reducing cortisol levels
    • 42 Factors increasing cortisol levels
  • 5 Biochemistry
    • 51 Biosynthesis
    • 52 Metabolism
  • 6 Chemistry
  • 7 Other animals
  • 8 See also
  • 9 References
  • 10 External links

Health effectsedit

Metabolic responseedit

In the early fasting state, cortisol stimulates gluconeogenesis the formation of glucose, and activates antistress and anti-inflammatory pathways Cortisol also plays an important, but indirect, role in liver and muscle glycogenolysis, the breaking down of glycogen to glucose-1-phosphate and glucose This is done through its passive influence on glucagonclarification needed Additionally, cortisol facilitates the activation of glycogen phosphorylase, which is necessary for epinephrine to have an effect on glycogenolysis45

In the late fasting state, the function of cortisol changes slightly and increases glycogenesis This response allows the liver to take up glucose not being used by the peripheral tissue and turn it into liver glycogen stores to be used if the body moves into the starvation statecitation needed

Elevated levels of cortisol, if prolonged, can lead to proteolysis breakdown of proteins and muscle wasting6 Several studies have shown that cortisol can have a lipolytic effect promote the breakdown of fat Under some conditions, however, cortisol may somewhat suppress lipolysis7

Immune responseedit

Cortisol prevents the release of substances in the body that cause inflammation It is used to treat conditions resulting from overactivity of the B-cell-mediated antibody response Examples include inflammatory and rheumatoid diseases, as well as allergies Low-potency hydrocortisone, available as a nonprescription medicine in some countries, is used to treat skin problems such as rashes and eczema

It inhibits production of interleukin IL-12, interferon IFN-gamma, IFN-alpha, and tumor-necrosis-factor TNF-alpha by antigen-presenting cells APCs and T helper Th1 cells, but upregulates IL-4, IL-10, and IL-13 by Th2 cells This results in a shift toward a Th2 immune response rather than general immunosuppression The activation of the stress system and resulting increase in cortisol and Th2 shift seen during an infection is believed to be a protective mechanism which prevents an over-activation of the inflammatory response8

Cortisol can weaken the activity of the immune system It prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 IL-1, and unable to produce the T-cell growth factor IL-29 Cortisol also has a negative-feedback effect on interleukin-110

Though IL-1 is useful in combating some diseases, endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels forcing the secretion of corticotropin-releasing hormone, thus antagonizing IL-1 The suppressor cells are not affected by glucosteroid response-modifying factor,11 so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin Rapid administration of corticosterone the endogenous type I and type II receptor agonist or RU28362 a specific type II receptor agonist to adrenalectomized animals induced changes in leukocyte distribution Natural killer cells are affected by cortisol12

Cortisol stimulates many copper enzymes often to 50% of their total potential, probably to increase copper availability for immune purposes13:337 This includes lysyl oxidase, an enzyme that cross-links collagen, and elastin13:334 Especially valuable for immune response is cortisol's stimulation of the superoxide dismutase,14 since this copper enzyme is almost certainly used by the body to permit superoxides to poison bacteria

Other effectsedit



Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis15 and inhibits the peripheral use of glucose insulin resistance15 by decreasing the translocation of glucose transporters especially GLUT4 to the cell membrane16 However, cortisol increases glycogen synthesis glycogenesis in the liver17 The permissive effect of cortisol on insulin action in liver glycogenesis is observed in hepatocyte culture in the laboratory, although the mechanism for this is unknown

Bone and collagenedit

Cortisol reduces bone formation,3 favoring long-term development of osteoporosis progressive bone disease It transports potassium out of cells in exchange for an equal number of sodium ions see above18 This can trigger the hyperkalemia of metabolic shock from surgery Cortisol also reduces calcium absorption in the intestine19

Collagen is an important component of connective tissue It is vital for structural support and is found in muscles, tendons, and joints, as well as throughout the entire body Cortisol down-regulates the synthesis of collagen20

Amino acidedit

Cortisol raises the free amino acids in the serum by inhibiting collagen formation, decreasing amino acid uptake by muscle, and inhibiting protein synthesis21 Cortisol as opticortinol may inversely inhibit IgA precursor cells in the intestines of calves22 Cortisol also inhibits IgA in serum, as it does IgM; however, it is not shown to inhibit IgE23

Wound healingedit

Cortisol and the stress response have known deleterious effects on the immune system High levels of perceived stress and increases in cortisol have been found to lengthen wound-healing time in healthy, male adults Those who had the lowest levels of cortisol the day following a 4 mm punch biopsy had the fastest healing time24 In dental students, wounds from punch biopsies took an average of 40% longer to heal when performed three days before an examination as opposed to biopsies performed on the same students during summer vacation25 This is in line with previous animal studies that show similar detrimental effects on wound healing, notably the primary reports showing that turtles recoil from cortisol26

Electrolyte balanceedit

Cortisol acts as a diuretic, increasing water diuresis, glomerular filtration rate, and renal plasma flow from the kidneys, as well as increasing sodium retention and potassium excretion It also increases sodium and water absorption and potassium excretion in the intestines27


Cortisol promotes sodium absorption through the small intestine of mammals28 Sodium depletion, however, does not affect cortisol levels29 so cortisol cannot be used to regulate serum sodium Cortisol's original purpose may have been sodium transport This hypothesis is supported by the fact that freshwater fish use cortisol to stimulate sodium inward, while saltwater fish have a cortisol-based system for expelling excess sodium30


A sodium load augments the intense potassium excretion by cortisol Corticosterone is comparable to cortisol in this case31 For potassium to move out of the cell, cortisol moves an equal number of sodium ions into the cell18 This should make pH regulation much easier unlike the normal potassium-deficiency situation, in which two sodium ions move in for each three potassium ions that move out—closer to the deoxycorticosterone effect

Stomach and kidneysedit

Cortisol stimulates gastric-acid secretion32 Cortisol's only direct effect on the hydrogen-ion excretion of the kidneys is to stimulate the excretion of ammonium ions by deactivating the renal glutaminase enzyme33


Cortisol works with epinephrine adrenaline to create memories of short-term emotional events; this is the proposed mechanism for storage of flash-bulb memories, and may originate as a means to remember what to avoid in the future34 However, long-term exposure to cortisol damages cells in the hippocampus;35 this damage results in impaired learning Furthermore, cortisol inhibits memory retrieval of already stored information3637

Sleep, stress, and moodedit

Diurnal cycles of cortisol levels are found in humans4 In humans, the amount of cortisol present in the blood undergoes diurnal variation; the level peaks in the early morning around 8 am and reaches its lowest level at about midnight-4 am, or three to five hours after the onset of sleep Information about the light/dark cycle is transmitted from the retina to the paired suprachiasmatic nuclei in the hypothalamus This pattern is not present at birth; estimates of when it begins vary from two weeks to nine months of age38

Changed patterns of serum cortisol levels have been observed in connection with abnormal ACTH levels, mood disorders such as major depressive disorder, anxiety disorders, psychological stress, and physiological stressors such as hypoglycemia, illness, fever, trauma, surgery, fear, pain, physical exertion, or temperature extremes Cortisol levels may also differ for individuals with autism or Asperger's syndrome39 Also, significant individual variation is seen, although a given person tends to have consistent rhythms

Effects during pregnancyedit

During human pregnancy, increased fetal production of cortisol between weeks 30 and 32 initiates production of fetal lung surfactant to promote maturation of the lungs In fetal lambs, glucocorticoids principally cortisol increase after about day 130, with lung surfactant increasing greatly, in response, by about day 135,40 and although lamb fetal cortisol is mostly of maternal origin during the first 122 days, 88% or more is of fetal origin by day 136 of gestation41 Although the timing of fetal cortisol concentration elevation in sheep may vary somewhat, it averages about 118 days before the onset of labor42 In several livestock species eg cattle, sheep, goats, and pigs, the surge of fetal cortisol late in gestation triggers the onset of parturition by removing the progesterone block of cervical dilation and myometrial contraction The mechanisms yielding this effect on progesterone differ among species In the sheep, where progesterone sufficient for maintaining pregnancy is produced by the placenta after about day 70 of gestation,4344 the prepartum fetal cortisol surge induces placental enzymatic conversion of progesterone to estrogen The elevated level of estrogen stimulates prostaglandin secretion and oxytocin receptor development

Exposure of fetuses to cortisol during gestation can have a variety of developmental outcomes, including alterations in prenatal and postnatal growth patterns In marmosets, a species of New World primates, pregnant females have varying levels of cortisol during gestation, both within and between females Infants born to mothers with high gestational cortisol during the first trimester of pregnancy had lower rates of growth in body mass indices than infants born to mothers with low gestational cortisol about 20% lower However, postnatal growth rates in these high-cortisol infants was more rapid than low-cortisol infants later in postnatal periods, and complete catch-up in growth had occurred by 540 days of age These results suggest that gestational exposure to cortisol in fetuses has important potential fetal programming effects on both pre- and postnatal growth in primates45

Synthesis and releaseedit

Cortisol is produced in the human body by the adrenal gland in the zona fasciculata,1 the second of three layers comprising the adrenal cortex The cortex forms the outer "bark" of each adrenal gland, situated atop the kidneys The release of cortisol is controlled by the hypothalamus, a part of the brain The secretion of corticotropin-releasing hormone by the hypothalamus46 triggers cells in the neighboring anterior pituitary to secrete another hormone, the adrenocorticotropic hormone ACTH, into the vascular system, through which blood carries it to the adrenal cortex ACTH stimulates the synthesis of cortisol, glucocorticoids, mineralocorticoids, and dehydroepiandrosterone

Normal levelsedit

Normal values indicated in the following tables pertain to humans normal levels vary among species Measured cortisol levels, and therefore reference ranges, depend on the analytical method used and factors such as age and sex Test results should, therefore, always be interpreted using the reference range from the laboratory that produced the result

Reference ranges for blood plasma content of free cortisol
Time Lower limit Upper limit Unit
09:00 am 14047 70047 nmol/L
548 2548 μg/dL
Midnight 8047 35047 nmol/l
2948 1348 μg/dl

Using the molecular weight of 362460 g/mole, the conversion factor from µg/dl to nmol/l is approximately 276; thus, 10 µg/dl is about 276 nmol/l

Reference ranges for urinalysis of free cortisol
Lower limit Upper limit Unit
2849 or 3050 28049 or 49050 nmol/24h
1051 or 1152 10051 or 17652 µg/24 h

Disorders of cortisol productionedit

  • Cushing's syndrome or hypercortisolism: Excessive levels of cortisol in the blood
  • Hypocortisolism: Insufficient levels of cortisol in the blood

Disorders of cortisol production, and some consequent conditions, are:

  • Primary hypercortisolism Cushing's syndrome
  • Primary hypocortisolism Addison's disease, Nelson's syndrome
    • Secondary hypercortisolism pituitary tumor resulting in Cushing's disease,5354 pseudo-Cushing's syndrome
    • Secondary hypocortisolism pituitary tumor, Sheehan's syndrome


The primary control of cortisol is the pituitary gland peptide, ACTH, which probably controls cortisol by controlling the movement of calcium into the cortisol-secreting target cells55 ACTH is in turn controlled by the hypothalamic peptide corticotropin-releasing hormone CRH, which is under nervous control CRH acts synergistically with arginine vasopressin, angiotensin II, and epinephrine56 In swine, which do not produce arginine vasopressin, lysine vasopressin acts synergistically with CRH57

When activated macrophages start to secrete IL-1, which synergistically with CRH increases ACTH,10 T-cells also secrete glucosteroid response modifying factor GRMF, as well as IL-1; both increase the amount of cortisol required to inhibit almost all the immune cells11 Immune cells then assume their own regulation, but at a higher cortisol setpoint The increase in cortisol in diarrheic calves is minimal over healthy calves, however, and falls over time58 The cells do not lose all their fight-or-flight override because of interleukin-1's synergism with CRH Cortisol even has a negative feedback effect on interleukin-110—especially useful to treat diseases that force the hypothalamus to secrete too much CRH, such as those caused by endotoxic bacteria The suppressor immune cells are not affected by GRMF,11 so the immune cells' effective setpoint may be even higher than the setpoint for physiological processes GRMF affects primarily the liver rather than the kidneys for some physiological processes59

High-potassium media which stimulates aldosterone secretion in vitro also stimulate cortisol secretion from the fasciculata zone of canine adrenals6061 — unlike corticosterone, upon which potassium has no effect62

Potassium loading also increases ACTH and cortisol in humans63 This is probably the reason why potassium deficiency causes cortisol to decline as mentioned and causes a decrease in conversion of 11-deoxycortisol to cortisol64 This may also have a role in rheumatoid-arthritis pain; cell potassium is always low in RA65

Ascorbic acid presence, particularly in high doses has also been shown to mediate stress response and decrease the levels of circulating cortisol in the body This can be evidenced through a decrease in systolic and diastolic blood pressures and through a decreased salivary cortisol level after treatment with ascorbic acid66

Factors reducing cortisol levelsedit

  • Magnesium supplementation decreases serum cortisol levels after aerobic exercise,6768 but not after resistance training69
  • Omega-3 fatty acids have a dose-dependent effect70 in slightly reducing cortisol release influenced by mental stress,71 suppressing the synthesis of interleukin-1 and -6 and enhancing the synthesis of interleukin-2; the former promotes higher CRH release Omega-6 fatty acids, though, have an inverse effect on interleukin synthesis72
  • Music therapy can reduce cortisol levels in certain situations73
  • Massage therapy can reduce cortisol74
  • Laughing, and the experience of humor, can lower cortisol levels75
  • Soy-derived phosphatidylserine interacts with cortisol; the correct dose, however, is unclear7677


  • Regular dancing has been shown to lead to significant decreases in salivary cortisol concentrations80
  • Withania somnifera ashwagandha root extract81
  • High-dosage treatment with ascorbic acid vitamin C has been shown to decrease circulating cortisol levels during and shortly after the treatment period66

Factors increasing cortisol levelsedit

  • Viral infections increase cortisol levels through activation of the HPA axis by cytokines82
  • Caffeine may increase cortisol levels83
  • Sleep deprivation84
  • Intense high VO2 max or prolonged aerobic exercise transiently increases cortisol levels to increase gluconeogenesis and maintain blood glucose;85 however, cortisol declines to normal levels after eating ie, restoring a neutral energy balance86
  • The Val/Val variation of the BDNF gene in men and the Val/Met variation in women are associated with increased salivary cortisol in a stressful situation87
  • Hypoestrogenism and melatonin supplementation increase cortisol levels in postmenopausal women88
  • Severe trauma or stressful events can elevate cortisol levels in the blood for prolonged periods89
  • Subcutaneous adipose tissue regenerates cortisol from cortisone by the enzyme 11-beta HSD190
  • Anorexia nervosa may be associated with increased cortisol levels91
  • The serotonin receptor gene 5HTR2C is associated with increased cortisol production in men92
  • Posing in low-power nonverbal displays through close, contractive postures can increase cortisol levels93
  • Smelling androstadienone has been found in one study to raise cortisol levels in women, as well as, in other studies, to affect mood see androstadienone article for details and citations
  • Excessive or problematic drinking has been linked to increased cortisol levels, especially in college students94



Steroidogenesis, showing cortisol at right95

Cortisol is synthesized from cholesterol Synthesis takes place in the zona fasciculata of the adrenal cortex The name cortisol is derived from cortex While the adrenal cortex also produces aldosterone in the zona glomerulosa and some sex hormones in the zona reticularis, cortisol is its main secretion in humans and several other species However, in cattle, corticosterone levels may approach96 or exceed4 cortisol levels The medulla of the adrenal gland lies under the cortex, mainly secreting the catecholamines adrenaline epinephrine and noradrenaline norepinephrine under sympathetic stimulation

The synthesis of cortisol in the adrenal gland is stimulated by the anterior lobe of the pituitary gland with ACTH; ACTH production is, in turn, stimulated by CRH, which is released by the hypothalamus ACTH increases the concentration of cholesterol in the inner mitochondrial membrane, via regulation of the steroidogenic acute regulatory protein It also stimulates the main rate-limiting step in cortisol synthesis, in which cholesterol is converted to pregnenolone and catalyzed by cytochrome P450SCC side-chain cleavage enzyme97


Cortisol is metabolized by the 11-beta hydroxysteroid dehydrogenase system 11-beta HSD, which consists of two enzymes: 11-beta HSD1 and 11-beta HSD2

  • 11-beta HSD1 uses the cofactor NADPH to convert biologically inert cortisone to biologically active cortisol
  • 11-beta HSD2 uses the cofactor NAD+ to convert cortisol to cortisone

Overall, the net effect is that 11-beta HSD1 serves to increase the local concentrations of biologically active cortisol in a given tissue; 11-beta HSD2 serves to decrease local concentrations of biologically active cortisol

Cortisol is also metabolized into 5-alpha tetrahydrocortisol 5-alpha THF and 5-beta tetrahydrocortisol 5-beta THF, reactions for which 5-alpha reductase and 5-beta reductase are the rate-limiting factors, respectively 5-Beta reductase is also the rate-limiting factor in the conversion of cortisone to tetrahydrocortisone

An alteration in 11-beta HSD1 has been suggested to play a role in the pathogenesis of obesity, hypertension, and insulin resistance known as metabolic syndrome98

An alteration in 11-beta HSD2 has been implicated in essential hypertension and is known to lead to the syndrome of apparent mineralocorticoid excess SAME


Cortisol is a naturally occurring pregnane corticosteroid and is also known as 11β,17α,21-trihydroxypregn-4-ene-3,20-dione

Other animalsedit

In non-human animals, cortisol is often used as an indicator of stress and can be measured in blood,99 saliva,100 urine,101 hair,102 and faeces102103

See alsoedit

  • Cortisone, a hormone
  • Membrane glucocorticoid receptor
  • List of corticosteroids


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External linksedit

  • Cortisol MS Spectrum
  • Cortisol serum/plasma at Lab Tests Online
  • Cortisol: analyte monograph – The Association for Clinical Biochemistry and Laboratory Medicine

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