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Cortisol
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This article is about the natural hormone. For the medication, see Hydrocortisone.
Not to be confused with cortisone, a metabolite from cortisol, with a similar name, genesis, and function.
This article's lead section may not adequately summarize its contents. To comply with Wikipedia's lead section guidelines, please consider modifying the lead to provide an accessible overview of the article's key points in such a way that it can stand on its own as a concise version of the article. (discuss). (November 2016)
Cortisol
Names
IUPAC name
11β,17α,21-Trihydroxypregn-4-ene-3,20-dione
Identifiers
CAS Number
50-23-7
3D model (JSmol)
Interactive image
ChEBI
CHEBI:17650
ChemSpider
5551
DrugBank
DB00741
ECHA InfoCard 100.000.019
KEGG
D00088
PubChem CID
5754
UNII
WI4X0X7BPJ
InChI[show]
InChI=1S/C21H30O5/c1-19-7-5-13(23)9-12(19)3-4-14-15-6-8-21(26,17(25)11-22)20(15,2)10-16(24)18(14)19/h9,14-16,18,22,24,26H,3-8,10-11H2,1-2H3/t14-,15-,16-,18+,19-,20-,21-/m0/s1
Key: JYGXADMDTFJGBT-VWUMJDOOSA-N
SMILES[show]
O=C4\C=C2/[C@]([C@H]1[C@@H](O)C[C@@]3([C@@](O)(C(=O)CO)CC[C@H]3[C@@H]1CC2)C)(C)CC4
Properties
Chemical formula
C21H30O5
Molar mass 362.460 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references
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 gland.[1] 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 carbohydrates.[2] It also decreases bone formation.[3]
Contents
[hide]
1 Health effects
1.1 Metabolic response
1.2 Immune response
2 Other effects
2.1 Metabolism
2.1.1 Glucose
2.1.2 Bone and collagen
2.1.3 Amino acid
2.2 Wound healing
2.3 Electrolyte balance
2.3.1 Sodium
2.3.2 Potassium
2.4 Stomach and kidneys
2.5 Memory
2.6 Sleep, stress, and mood
2.7 Effects during pregnancy
3 Synthesis and release
3.1 Normal levels
3.2 Disorders of cortisol production
4 Regulation
4.1 Factors reducing cortisol levels
4.2 Factors increasing cortisol levels
5 Biochemistry
5.1 Biosynthesis
5.2 Metabolism
6 Chemistry
7 Other animals
8 See also
9 References
10 External links
Health effects[edit]
Metabolic response[edit]
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 glucagon.[clarification needed] Additionally, cortisol facilitates the activation of glycogen phosphorylase, which is necessary for epinephrine to have an effect on glycogenolysis.[4][5]
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 state.[citation needed]
Elevated levels of cortisol, if prolonged, can lead to proteolysis (breakdown of proteins) and muscle wasting.[6] Several studies have shown that cortisol can have a lipolytic effect (promote the breakdown of fat). Under some conditions, however, cortisol may somewhat suppress lipolysis.[7]
Immune response[edit]
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 (Th)1 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 response.[8]
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-2).[9] Cortisol also has a negative-feedback effect on interleukin-1.[10]
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 cortisol.[12]
Cortisol stimulates many copper enzymes (often to 50% of their total potential), probably to increase copper availability for immune purposes.[13]:337 This includes lysyl oxidase, an enzyme that cross-links collagen, and elastin.[13]: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 effects[edit]
Metabolism[edit]
Glucose[edit]
Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis[15] and inhibits the peripheral use of glucose (insulin resistance)[15] by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane.[16] However, cortisol increases glycogen synthesis (glycogenesis) in the liver.[17] 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 collagen[edit]
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 above).[18] This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine.[19]
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 collagen.[20]
Amino acid[edit]
Cortisol raises the free amino acids in the serum by inhibiting collagen formation, decreasing amino acid uptake by muscle, and inhibiting protein synthesis.[21] Cortisol (as opticortinol) may inversely inhibit IgA precursor cells in the intestines of calves.[22] Cortisol also inhibits IgA in serum, as it does IgM; however, it is not shown to inhibit IgE.[23]
Wound healing[edit]
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 time.[24] 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 vacation.[25] 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 cortisol.[26]
Electrolyte balance[edit]
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 intestines.[27]
Sodium[edit]
Cortisol promotes sodium absorption through the small intestine of mammals.[28] Sodium depletion, however, does not affect cortisol levels[29] 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 sodium.[30]
Potassium[edit]
A sodium load augments the intense potassium excretion by cortisol. Corticosterone is comparable to cortisol in this case.[31] For potassium to move out of the cell, cortisol moves an equal number of sodium ions into the cell.[18] 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 kidneys[edit]
Cortisol stimulates gastric-acid secretion.[32] 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 enzyme.[33]
Memory[edit]
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 future.[34] 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 information.[36][37]
Sleep, stress, and mood[edit]
Diurnal cycles of cortisol levels are found in humans.[4] 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 age.[38]
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 syndrome.[39] Also, significant individual variation is seen, although a given person tends to have consistent rhythms.
Effects during pregnancy[edit]
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 gestation.[41] Although the timing of fetal cortisol concentration elevation in sheep may vary somewhat, it averages about 11.8 days before the onset of labor.[42] In several livestock species (e.g. 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,[43][44] 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 primates.[45]
Synthesis and release[edit]
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 hypothalamus[46] 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 levels[edit]
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 140[47] 700[47] nmol/L
5[48] 25[48] μg/dL
Midnight 80[47] 350[47] nmol/l
2.9[48] 13[48] μg/dl
Using the molecular weight of 362.460 g/mole, the conversion factor from µg/dl to nmol/l is approximately 27.6; thus, 10 µg/dl is about 276 nmol/l.
Reference ranges for urinalysis of free cortisol
Lower limit
Upper limit
Unit
28[49] or 30[50] 280[49] or 490[50] nmol/24h
10[51] or 11[52] 100[51] or 176[52] µg/24 h
Disorders of cortisol production[edit]
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,[53][54] pseudo-Cushing's syndrome)
Secondary hypocortisolism (pituitary tumor, Sheehan's syndrome)
Regulation[edit]
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 cells.[55] 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 epinephrine.[56] (In swine, which do not produce arginine vasopressin, lysine vasopressin acts synergistically with CRH.[57])
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 cells.[11] 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 time.[58] 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-1[10]—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 processes.[59]
High-potassium media (which stimulates aldosterone secretion in vitro) also stimulate cortisol secretion from the fasciculata zone of canine adrenals[60][61] — unlike corticosterone, upon which potassium has no effect.[62]
Potassium loading also increases ACTH and cortisol in humans.[63] This is probably the reason why potassium deficiency causes cortisol to decline (as mentioned) and causes a decrease in conversion of 11-deoxycortisol to cortisol.[64] This may also have a role in rheumatoid-arthritis pain; cell potassium is always low in RA.[65]
Ascorbic acid presence, particularly in high doses has also been shown to mediate response to psychological stress and speed the decrease of the levels of circulating cortisol in the body post stress. This can be evidenced through a decrease in systolic and diastolic blood pressures and decreased salivary cortisol level after treatment with ascorbic acid.[66]
Factors reducing cortisol levels[edit]
Magnesium supplementation decreases serum cortisol levels after aerobic exercise,[67][68] but not after resistance training.[69]
Omega-3 fatty acids have a dose-dependent effect[70] 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 synthesis.[72]
Music therapy can reduce cortisol levels in certain situations.[73]
Massage therapy can reduce cortisol.[74]
Laughing, and the experience of humor, can lower cortisol levels.[75]
Soy-derived phosphatidylserine interacts with cortisol; the correct dose, however, is unclear.[76][77][78][79]
Regular dancing has been shown to lead to significant decreases in salivary cortisol concentrations.[80]
Withania somnifera (ashwagandha) root extract[81]
High-dosage treatment with ascorbic acid (vitamin C) has been shown to decrease circulating cortisol levels during and shortly after the treatment period.[66]
Factors increasing cortisol levels[edit]
Viral infections increase cortisol levels through activation of the HPA axis by cytokines.[82]
Caffeine may increase cortisol levels.[83]
Sleep deprivation[84]
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 (i.e., restoring a neutral energy balance)[86]
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 situation.[87]
Severe trauma or stressful events can elevate cortisol levels in the blood for prolonged periods.[88]
Subcutaneous adipose tissue regenerates cortisol from cortisone by the enzyme 11-beta HSD1.[89]
Anorexia nervosa may be associated with increased cortisol levels.[90]
The serotonin receptor gene 5HTR2C is associated with increased cortisol production in men.[91]
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 students.[92]
Biochemistry[edit]
Biosynthesis[edit]
Steroidogenesis, showing cortisol at right.[93]
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 approach[94] or exceed[4] 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 enzyme).[95]
Metabolism[edit]
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 syndrome.[96]
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).
Chemistry[edit]
Cortisol is a naturally occurring pregnane corticosteroid and is also known as 11β,17α,21-trihydroxypregn-4-ene-3,20-dione.
Other animals[edit]
In non-human animals, cortisol is often used as an indicator of stress and can be measured in blood,[97] saliva,[98] urine,[99] hair,[100] and faeces.[100][101]
See also[edit]
Cortisone, a hormone
Membrane glucocorticoid receptor
List of corticosteroids
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^ Jump up to: a b c d Biochemistry Reference Ranges at Good Hope Hospital Retrieved 8 November 2009[better source needed]
^ Jump up to: a b c d Derived from molar values using molar mass of 362 g/mol
^ Jump up to: a b Converted from µg/24h, using molar mass of 362.460 g/mol
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^ Jump up to: a b MedlinePlus Encyclopedia Cortisol – urine
^ Jump up to: a b Converted from nmol/24h, using molar mass of 362.460 g/mol
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External links[edit]
Wikimedia Commons has media related to Cortisol.
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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18-Hydroxy-11-deoxycorticosterone
18-Hydroxycorticosterone
18-Hydroxyprogesterone
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16α-Hydroxy-DHEA sulfate
Testosterone
Metabolites: 3α-Androstanediol
3α-Androstanediol glucuronide
3β-Androstanediol
3α,5β-Androstanediol
3β,5β-Androstanediol
5β-Androstanedione
5β-Dihydrotestosterone
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2-Hydroxyestradiol
2-Hydroxyestriol
2-Hydroxyestrone
4-Hydroxyestradiol
4-Hydroxyestriol
4-Hydroxyestrone
4-Methoxyestradiol
16α-Hydroxyestrone
Others: 27-Hydroxycholesterol
3α-Androstanediol
3β-Androstanediol
4-Androstenedione
5-Androstenediol
DHEA
DHEA sulfate
7-Keto-DHEA
7α-Hydroxy-DHEA
16α-Hydroxy-DHEA
Metabolites: 2-Methoxyestradiol
2-Methoxyestrone
4-Methoxyestrone
Estradiol glucuronide
Estradiol sulfate
Estrone glucuronide
Estrone sulfate
Estriol glucuronide
Estriol sulfate
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Progesterone
16α-Hydroxyprogesterone
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5α-DHDOC
Metabolites: Allopregnanediol
Pregnanediol
Pregnanediol glucuronide
Pregnanetriol
Neurosteroids
Cholestanes: 24S-Hydroxycholesterol
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Pregnanes: 3α-Dihydroprogesterone
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5α-Dihydroprogesterone
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11-Deoxycorticosterone
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Pregnenolone
Pregnenolone sulfate
Progesterone
THB
THDOC
Androstanes: 3α-Androstanediol
3α-Androstenol
7-Keto-DHEA
7α-Hydroxy-DHEA
7β-Hydroxy-DHEA
7α-Hydroxyepiandrosterone
7β-Hydroxyepiandrosterone
Androsterone
DHEA
DHEA sulfate
Etiocholanolone
Pheromones: 3α-Androstenol
3β-Androstenol
Androstadienol
Androstadienone
Androstenone
Androsterone
Estratetraenol
Others
Vitamin D: 7-Dehydrocholesterol
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Cholecalciferol
Others: 7α-Hydroxycholesterol
11α-Hydroxyprogesterone
11β-Hydroxyprogesterone
Cholesterol sulfate
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Glucocorticoid receptor modulators
GR
Agonists
Cortisol-like and related (16-unsubstituted): 3α,5α-Tetrahydrocorticosterone
5α-Dihydrocorticosterone
9α-Fluorocortisone (alfluorone)
11-Dehydrocorticosterone (11-oxocorticosterone, 17-deoxycortisone)
11-Dehydrocorticosterone acetate
11-Deoxycorticosterone (desoxycortone, deoxycortone, desoxycorticosterone)
Desoxycortone esters
11-Deoxycortisol (cortodoxone, cortexolone)
Cortifen (cortiphen, kortifen)
Cortodoxone acetate
21-Deoxycortisol
Δ7-Prednisolone
Δ7-Prednisolone 21-acetate
Amebucort
Chloroprednisone
Chloroprednisone acetate
Cloprednol
Cloprednol acetate
Corticosterone
Corticosterone acetate
Corticosterone benzoate
Cortisol (hydrocortisone)
Benzodrocortisone (hydrocortisone benzoate)
Hydrocortamate (hydrocortisone diethylaminoacetate)
Hydrocortisone esters
Cortisone
Cortisone acetate
Deprodone
Deprodone propionate
Dichlorisone
Dichlorisone acetate
Dichlorisone diacetate
Difluprednate
Endrisone (endrysone)
Etiprednol
Etiprednol dicloacetate (etiprednol dichloroacetate)
Fludrocortisone (fludrocortone)
Fludrocortisone acetate
Fluorometholone
Fluorometholone acetate
Fluperolone
Fluperolone acetate
Fluprednisolone
Fluprednisolone esters
Halopredone
Halopredone acetate (halopredone diacetate)
Isoflupredone (9α-fluoroprednisolone)
Isoflupredone acetate
Loteprednol
Loteprednol etabonate
Mazipredone (depersolone)
Medrysone
Methylprednisolone
Methylprednisolone esters
Prebediolone
Prebediolone acetate
Prednisolone
Prednazate
Prednazoline
Prednicarbate (prednisolone ethylcarbonate propionate)
Prednimustine
Prednisolamate (prednisolone diethylaminoacetate)
Prednisolone esters
Prednisone
Prednisone esters
Pregnenolone
Pregnenolone acetate
Pregnenolone succinate (pregnenolone hemisuccinate)
Resocortol
Tipredane
Tixocortol
Butixocort (tixocortol butyrate)
Butixocort propionate
Tixocortol pivalate
Methasones and related (16-substituted): 16α-Methyl-11-oxoprednisolone
Alclometasone
Alclometasone dipropionate
Amelometasone
Beclometasone (beclomethasone)
Beclometasone esters
Betamethasone (betametasone)
Betamethasone esters
Cortobenzolone (betamethasone salicylate)
Ciclometasone (ciclomethasone, cyclomethasone)
Clobetasol
Clobetasol propionate
Clobetasone
Clobetasone butyrate
Clocortolone
Clocortolone esters
Cloticasone
Cloticasone propionate
Cormetasone (cormethasone)
Cormetasone acetate
Descinolone
Desoximetasone (desoxymethasone)
Dexamethasone (dexametasone)
Dexamethasone esters
Diflorasone
Diflorasone diacetate
Diflucortolone
Diflucortolone pivalate
Diflucortolone valerate
Dimesone
Dimesone acetate
Doxibetasol (doxybetasol)
Fluclorolone
Flumetasone (flumethasone)
Flumetasone acetate
Flumetasone pivalate
Fluocinolone
Fluocortin
Fluocortin butyl (fluocortin butylate)
Fluocortolone
Fluocortolone esters
Fluprednidene (fluprednylidene)
Fluprednidene acetate
Fluticasone
Fluticasone furoate
Fluticasone propionate
Halocortolone
Halometasone
Icometasone
Icometasone enbutate (icometasone butyrate acetate)
Isoprednidene
Locicortolone (locicortone)
Locicortolone dicibate (locicortone dicibate)
Meclorisone
Meclorisone dibutyrate
Meprednisone (methylprednisone)
Meprednisone acetate
Meprednisone hydrogen succinate (methylprednisone hemisuccinate)
Mometasone
Mometasone furoate
Paramethasone
Paramethasone acetate
Paramethasone disodium phosphate
Paramethasone phosphate
Prednylidene
Prednylidene diethylaminoacetate
Rimexolone
Ticabesone
Ticabesone propionate
Timobesone
Timobesone acetate
Triamcinolone
Triamcinolone diacetate
Ulobetasol (halobetasol)
Ulobetasol propionate
Vamorolone
Cyclic ketals (16,17-cyclized): Acrocinonide (triamcinolone acroleinide)
Amcinafal (triamcinolone pentanonide)
Amcinafide (triamcinolone acetophenide)
Amcinonide (triamcinolone acetate cyclopentanonide)
Budesonide
Ciclesonide
Cicortonide
Deflazacort (azacort)
Descinolone acetonide
Desonide (hydroxyprednisolone acetonide)
Desonide disodium phosphate
Desonide pivalate
Dexbudesonide
Drocinonide
Drocinonide phosphate
Fluazacort
Fluclorolone acetonide (flucloronide)
Fludroxycortide (flurandrenolone, flurandrenolide)
Flumoxonide
Flunisolide
Flunisolide acetate
Fluocinolone acetonide
Ciprocinonide (fluocinolone acetonide cyclopropylcarboxylate)
Fluocinonide (fluocinolide, fluocinolone acetonide acetate)
Procinonide (fluocinolone acetonide propionate)
Formocortal
Halcinonide
Itrocinonide
Rofleponide
Rofleponide palmitate
Tralonide
Triamcinolone acetonide
Flupamesone (triamcinolone acetonide metembonate)
Triamcinolone acetonide esters
Triamcinolone aminobenzal benzamidoisobutyrate (TBI-PAB)
Triclonide
Others/atypical (other expanded steroid ring systems, homosteroids, and non-pregnane steroids): Cortisuzol
Cortivazol
Domoprednate
Naflocort
Nicocortonide
Nicocortonide acetate
Nivacortol (nivazol)
Oxisopred
RU-28362
Non-corticosteroids with some glucocorticoid activity: 15β-Hydroxycyproterone acetate
17α-Hydroxyprogesterone
Chlormadinone acetate
Cyproterone
Cyproterone acetate
Delmadinone acetate
Desogestrel
Flugestone
Flugestone acetate (flurogestone acetate)
Fluoxymesterone
Gestodene
Medrogestone
Medroxyprogesterone acetate
Megestrol acetate
Metribolone
Norgestomet
Osaterone acetate
Progesterone
Promegestone
Quingestrone
Segesterone acetate (nestorone)
Tetrahydrogestrinone
Nonsteroidal glucocorticoids: AZD-5423
GSK-9027
Mixed
(SEGRMs)
Dagrocorat
Fosdagrocorat
Mapracorat
Antagonists
7α-Hydroxy-DHEA
17α-Methylprogesterone
Aglepristone
Asoprisnil
Asoprisnil ecamate
C108297
C113176
CORT-108297
Cyproterone acetate
Guggulsterone
Ketoconazole
Lilopristone
LLY-2707
Metapristone (RU-42633)
Miconazole
Mifepristone (RU-486)
Onapristone
ORG-34116
ORG-34517 (SCH-900636)
ORG-34850
Pregnenolone 16α-carbonitrile
Relacorilant (CORT-125134)
RTI 3021–012
RTI 3021–022
Telapristone
Tibolone
Toripristone
Ulipristal acetate
Others
Antisense oligonucleotides: IONIS-GCCRRx (ISIS-426115)
See also
Receptor/signaling modulators
Glucocorticoids and antiglucocorticoids
Mineralocorticoid receptor modulators
List of corticosteroids
[show]
v
t
e
Mineralocorticoid receptor modulators
MR
Agonists
11-Dehydrocorticosterone (11-oxocorticosterone, 17-deoxycortisone)
11-Dehydrocorticosterone acetate
11-Deoxycorticosterone (desoxycortone, deoxycortone, desoxycorticosterone)
Desoxycortone esters
11-Deoxycortisol (cortodoxone, cortexolone)
Cortifen (cortiphen, kortifen)
Cortodoxone acetate
11β-Hydroxyprogesterone
16α,18-Dihydroxy-11-deoxycorticosterone
17α-Hydroxyaldosterone
18-Hydroxy-11-deoxycorticosterone
19-Norprogesterone
Aldosterone
Corticosterone
Corticosterone acetate
Corticosterone benzoate
Cortisol (hydrocortisone)
Benzodrocortisone (hydrocortisone benzoate)
Hydrocortamate (hydrocortisone diethylaminoacetate)
Hydrocortisone esters
Cortisone
Cortisone acetate
Fludrocortisone (fludrocortone)
Fludrocortisone acetate
Mometasone
Mometasone furoate
Prednisolone
Prednazate
Prednazoline
Prednicarbate (prednisolone ethylcarbonate propionate)
Prednimustine
Prednisolamate (prednisolone diethylaminoacetate)
Prednisolone esters
Prednisone
Prednisone esters
Antagonists
Steroidal: 6β-Hydroxy-7α-thiomethylspironolactone
7α-Thiomethylspironolactone (SC-26519)
7α-Thioprogesterone (SC-8365)
7α-Thiospironolactone (SC-24813)
16α-Hydroxyprogesterone
17α-Hydroxyprogesterone
18-Deoxyaldosterone
Canrenoate potassium (potassium canrenoate)
Canrenoic acid (canrenoate)
Canrenone (canrenoate y-lactone)
Dicirenone
Dimethisterone
Drospirenone
Dydrogesterone
Eplerenone
Gestodene
Guggulsterone
Medrogestone
Mespirenone
Mexrenoate potassium
Mexrenoic acid (mexrenoate)
Mexrenone
Oxprenoic acid (oxprenoate)
Oxprenoate potassium (RU-28318)
Pregnenolone
Progesterone
Prorenoate potassium
Prorenoic acid (prorenoate)
Prorenone
RO-14-9012
RU-26752
SC-5233 (spirolactone)
SC-8109
SC-11927 (CS-1)
SC-19886
SC-27169
Spirorenone
Spironolactone
Spiroxasone
Tibolone
Trimegestone
ZK-91587
ZK-97894
Nonsteroidal: Amlodipine
Apararenone
Benidipine
BR-4628
Esaxerenone
Felodipine
Finerenone
Nifedipine
Nimodipine
Nitrendipine
PF-03882845
SM-368229
See also
Receptor/signaling modulators
Mineralocorticoids and antimineralocorticoids
Glucocorticoid receptor modulators
List of corticosteroids
Authority control
LCCN: sh85063384
GND: 4160902-5
Retrieved from "https://en.wikipedia.org/w/index.php?title=Cortisol&oldid=821809039"
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text:
Where Am I Going?
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Where Am I Going?
Studio album by Dusty Springfield
Released
27 October 1967
Recorded
July–August 1967 (Track A4: November 1965)
Studio
Philips Studios, Stanhope Place, London
Genre
Pop
Length
31:20
Label
Philips
BL 7820 (mono)
SBL 7820 (stereo)
Producer
Johnny Franz
Dusty Springfield (Track A5)
Dusty Springfield chronology
Ev'rything's Coming Up Dusty
(1965)Ev'rything's Coming Up Dusty1965 Where Am I Going?
(1967) Dusty... Definitely
(1968)Dusty... Definitely1968
Professional ratings
Review scores
Source
Rating
Allmusic [1]
Where Am I Going? is the third studio album by singer Dusty Springfield, released on Philips Records in the UK in 1967. By now, firmly established as one of the most popular singers in Britain, with several hits in America as well, Springfield ventured into more varying styles than before and recorded a wide variety of material for this album. Rather than the straightforward pop of A Girl Called Dusty or the mix of pop and soul of Ev'rything's Coming Up Dusty, Springfield recorded a variety of styles from jazz to soul, to pop and even show tunes (the standout title track, from the musical Sweet Charity). While not the success that her previous two albums were, Where Am I Going? was praised by fans and critics alike for showing a mature and sophisticated sensibility, despite the many different styles of music.
In the United States, the album was released in a quite altered form as The Look of Love, titled after a successful Springfield recording originally only released as a single B-side in Britain. Also included were two other singles — "Give Me Time", a U.K. and United States hit, and "What's It Gonna Be", a United States hit — not included on Where Am I Going?. The Look of Love also contained the UK single B-side "Small Town Girl", not on Where Am I Going?.
Where Am I Going? was released to CD for the first time in the early 1990s. A digitally remastered edition was released in 1998, and included the bonus tracks "I've Got a Good Thing", "Don't Forget About Me" (a later version appeared on Dusty in Memphis), and "Time After Time".
"Where Am I Going?" was sampled in the song "Zenophile", from the 2004 album Destroy Rock & Roll, by Scottish electronic music artist Mylo. "I Can't Wait Until I See My Baby's Face" was sampled in the song "Nothing Can Stop Us" from the 1991 album Foxbase Alpha by Saint Etienne.
Track listing[edit]
Side A
"Bring Him Back" (Mort Shuman, Doc Pomus) - 2:12
"Don't Let Me Lose This Dream" (Aretha Franklin, Ted White) - 2:24
"I Can't Wait Until I See My Baby's Face" (Jerry Ragovoy, Chip Taylor) - 2:39
"Take Me for a Little While" (Trade Martin) - 2:22
"Chained to a Memory" (Kay Rogers, Richard Ahlert) - 2:35
"Sunny" (Bobby Hebb) - 1:52
Side B
"(They Long to Be) Close to You" (Burt Bacharach, Hal David) - 2:25
"Welcome Home" (Chip Taylor) - 2:38
"Come Back to Me" (Alan Jay Lerner, Burton Lane) - 2:03
"If You Go Away (Ne Me Quitte Pas)" (Jacques Brel, Rod McKuen) - 3:50
"Broken Blossoms" (Traditional, Tom Springfield, Robert Gray) - 2:41
"Where Am I Going?" (Dorothy Fields, Cy Coleman) - 3:39
Bonus tracks 1998 CD re-issue
"I've Got a Good Thing" (Jerry Ragovoy, Mort Shuman) - 2:49
Outtake from the Where Am I Going? sessions. First release: UK compilation Something Special, 1996.
"Don't Forget About Me" (London recording) (Gerry Goffin, Carole King) - 2:49
Outtake from the Where Am I Going? sessions. First release: UK compilation Something Special, 1996.
"Time After Time" (Jule Styne, Sammy Cahn) - 2:30
Outtake from the Where Am I Going? sessions. First release: UK 4-CD box set The Legend of Dusty Springfield, 1994.
Track 13: Originally recorded in New York 1965, producer: Jerry Ragovoy. Additional overdubs / re-recording London 1967, producer: Johnny Franz.
Track 14: Re-recorded in 1968 for album Dusty in Memphis.
Tracks 14-15: Producer: Johnny Franz.
Personnel and production[edit]
Dusty Springfield - lead vocals, backing vocals
Lesley Duncan - backing vocals
Madeline Bell - backing vocals
The Echoes - accompaniment
Alan Tew - accompaniment & orchestra director
Arthur Greenslade - accompaniment & orchestra director
Wally Stott - accompaniment & orchestra director
Peter Knight - accompaniment & orchestra director
Reg Guest - accompaniment & orchestra director
Pat Williams - musical arranger
Jim Tyler - musical arranger
Johnnie Spence - musical arranger
Johnny Franz - record producer
Roger Wake - digital remastering/remix (1998 re-issue)
Mike Gill - digital remastering/remix (1998 re-issue)
References[edit]
Jump up ^ Allmusic review
Howes, Paul (2001). The Complete Dusty Springfield. London: Reynolds & Hearn Ltd. ISBN 1-903111-24-2.
[hide]
v
t
e
Dusty Springfield
UK studio albums (1964–68)
A Girl Called Dusty (1964)
Ev'rything's Coming Up Dusty (1965)
Where Am I Going? (1967)
Dusty... Definitely (1968)
US studio albums (1964–68)
Stay Awhile/I Only Want to Be with You (1964)
Dusty (1964)
Ooooooweeee!!! (1965)
You Don't Have to Say You Love Me (1966)
The Look of Love (1967)
Studio albums (1969–)
Dusty in Memphis (1969)
A Brand New Me/From Dusty with Love (1970)
See All Her Faces (1972)
Cameo (1973)
Longing (unreleased, recorded 1974)
It Begins Again (1977)
Living Without Your Love (1979)
White Heat (1982)
Reputation (1990)
A Very Fine Love (1995)
Faithful (2015, recorded 1971)
Other
Discography
Retrieved from "https://en.wikipedia.org/w/index.php?title=Where_Am_I_Going%3F&oldid=835119808"
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Dusty Springfield albums
1967 albums
Albums produced by Johnny Franz
Philips Records albums
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This page was last edited on 6 April 2018, at 17:43.
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