HGH Injections For Sale

When it comes to building speed, strength, and recovery, growth hormone (GH), and more specifically human growth hormone (hGH), has often been touted as one way to get an edge. Athletes, however, should know the risks associated with growth hormone from a health and clean sport perspective.

Humans naturally produce growth hormone, which controls how the body grows from childhood to adulthood but doesnt directly act on the bones and muscles. When growth hormone is released by the pituitary in the brain, it circulates in the blood and stimulates the release of a protein called IGF-1 from the liver. The IGF-1 protein is what ultimately stimulates the growth of bones, muscle, and other tissues.

Growth hormone levels are highest in children and decrease with age. While adults still produce growth hormone, the levels are much lower than in children and adolescents.

Yes. Growth hormone is in the category of Anabolic Agents on the World Anti-Doping Agency (WADA) Prohibited List and is prohibited at all times and for all levels of athletes, including elite, junior, and masters-level athletes. Even if you are prescribed growth hormone by a doctor for one of the conditions mentioned below, an approved Therapeutic Use Exemption (TUE) is required to use growth hormone in sport.

Growth hormone may only be legally prescribed for a small number of conditions. In pediatric patients, doctors can prescribe it to treat growth hormone deficiency, Prader-Willi syndrome, Turner syndrome, idiopathic short stature (when children are smaller than normal but there isnt a clear reason) and to treat growth failure in children born small who dont catch up by the time they are two.

In adults, growth hormone can also be prescribed to treat growth hormone deficiency as a result of pituitary disease, radiation therapy, or trauma. However, the medical use of growth hormone is complex because determining the right time to give the medication and figuring out who will actually benefit from it can be subjective. Growth hormone does not always cause a measurable increase in the rate of growth or development.

The use of growth hormone for an off-label use (not approved by the Food and Drug Administration) is unlawful and a felony under the Food, Drug, and Cosmetic Act. According to a statement by the Drug Enforcement Agency, growth hormone that is sold for wellness or anti-aging purposes is marketed, distributed, and illegally prescribed off-label to aging adults to replenish declining hGH levels and reverse age-related bodily deterioration.

Some wellness or anti-aging clinics also prescribe drugs that cause the body to release more growth hormone, such as growth hormone releasing hormone (GHRH) and other factors. Many compounds that are advertised to have these effects are investigational new drugs that are not yet approved by the FDA. Under the WADA Prohibited List, growth hormone releasing factors are prohibited at all times.

Athletes should check the anti-doping status of any medication they are prescribed on GlobalDRO.com before using them in sport.

Dietary supplements that claim to contain growth hormone or that advertise to cause the release of growth hormone should be avoided by athletes. The use of any dietary supplement is at the athletes own risk.

There are many reported side effects from the use of growth hormone, including irritation at the injection site, increased blood pressure in the brain, damage to the retina and vision in people with diabetes, damage to the growth plates in the femur in pediatric patients, faster progression of scoliosis in people who have this condition, hypothyroidism, pancreatitis, swelling or stiffness in the arms and legs, and generalized pain.

Long-term, the use of growth hormone may cause the body to stop producing its own, or to downregulate the growth hormone pathways.

For questions about specific products, substances, and methods, contact USADAs Drug Reference Line at drugreference@usada.org or call (719) 785-2000, option 2.

Excerpt from:

Growth Hormone in Sport: What Athletes Should Know | USADA

Human natural glucocorticoid hormone

11,17,21-Trihydroxypregn-4-ene-3,20-dione

(1R,3aS,3bS,9aR,9bS,11aS)-1,10-Dihydroxy-1-(hydroxyacetyl)-9a,11a-dimethyl-1,2,3,3a,3b,4,5,8,9,9a,9b,10,11,11a-tetradecahydro-7H-cyclopenta[a]phenanthen-7-one

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

O=C4C=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

Chemical compound

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 many animals, mainly by the zona fasciculata of the adrenal cortex in the adrenal gland.[1][bettersourceneeded] It is produced in other tissues in lower quantities.[2] It is released with a diurnal cycle and its release is increased 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.[3] It also decreases bone formation.[4] Many of these functions are carried out by cortisol binding to glucocorticoid or mineralocorticoid receptors inside the cell, which then bind to DNA to impact gene expression.[5][6]

In general, cortisol stimulates gluconeogenesis (the synthesis of 'new' glucose from non-carbohydrate sources, which occurs mainly in the liver, but also in the kidneys and small intestine under certain circumstances). The net effect is an increase in the concentration of glucose in the blood, further complemented by a decrease in the sensitivity of peripheral tissue to insulin, thus preventing this tissue from taking the glucose from the blood. Cortisol has a permissive effect on the actions of hormones that increase glucose production, such as glucagon and adrenaline.[7]

Cortisol also plays an important, but indirect, role in liver and muscle glycogenolysis (the breaking down of glycogen to glucose-1-phosphate and glucose) which occurs as a result of the action of glucagon and adrenaline. Additionally, cortisol facilitates the activation of glycogen phosphorylase, which is necessary for adrenaline to have an effect on glycogenolysis.[8][9]

Paradoxically, cortisol promotes not only gluconeogenesis in the liver, but also glycogenesis. Cortisol is thus better thought of as stimulating glucose/glycogen turnover in the liver.[10] This is in contrast to cortisol's effect in the skeletal muscle where glycogenolysis is promoted indirectly through catecholamines.[11]

Elevated levels of cortisol, if prolonged, can lead to proteolysis (breakdown of proteins) and muscle wasting.[12] The reason for proteolysis is to provide the relevant tissue with a feedstock for gluconeogenesis; see glucogenic amino acids.[7] The effects of cortisol on lipid metabolism are more complicated since lipogenesis is observed in patients with chronic, raised circulating glucocorticoid (i.e. cortisol) levels,[7] although an acute increase in circulating cortisol promotes lipolysis.[13] The usual explanation to account for this apparent discrepancy is that the raised blood glucose concentration (through the action of cortisol) will stimulate insulin release. Insulin stimulates lipogenesis, so this is an indirect consequence of the raised cortisol concentration in the blood but it will only occur over a longer time scale.

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-dose topical hydrocortisone, available as a nonprescription medicine in some countries, is used to treat skin problems such as rashes and eczema.

Cortisol inhibits production of interleukin 12 (IL-12), interferon gamma (IFN-gamma), IFN-alpha, and tumor necrosis factor alpha (TNF-alpha) by antigen-presenting cells (APCs) and T helper cells (Th1 cells), but upregulates interleukin 4, interleukin 10, and interleukin 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.[14]

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, and unable to produce the T-cell growth factor IL-2. Cortisol downregulates the expression of the IL2 receptor IL-2R on the surface of the helper T-cell which is necessary to induce a Th1 'cellular' immune response, thus favoring a shift towards Th2 dominance and the release of the cytokines listed above which results in Th2 dominance and favors the 'humoral' B-cell mediated antibody immune response).[15]

Cortisol also has a negative-feedback effect on IL-1.[16]The way this negative feedback works is that an immune stressor causes peripheral immune cells to release IL-1 and other other cytokines such as IL-6 and TNF-alpha. These cytokines stimulate the hypothalamus, causing it to release corticotropin-releasing hormone (CRH). CRH in turn stimulates the production of adrenocorticotropic hormone (ACTH) among other things in the adrenal gland, which (among other things) increases production of cortisol. Cortisol then closes the loop as it inhibits TNF-alpha production in immune cells and makes them less responsive to IL-1.[17]

Through this system, as long as an immune stressor is small, the response will be regulated to the correct level. Like a thermostat controlling a heater, the hypothalamus uses cortisol to turn off the heat once the production of cortisol matches the stress induced on the immune system. But in a severe infection or in a situation where the immune system is overly sensitized to an antigen (such as in allergic reactions) or there is a massive flood of antigens (as can happen with endotoxic bacteria) the correct set point might never be reached. Also because of downregulation of Th1 immunity by cortisol and other signaling molecules, certain types of infection, (notably Mycobacterium tuberculosis) can trick the body into getting locked in the wrong mode of attack, using an antibody-mediated humoral response when a cellular response is needed.

Lymphocytes are the antibody-producing cells of the body, and are thus the main agents of humoral immunity. A larger number of lymphocytes in the lymph nodes, bone marrow, and skin means the body is increasing its humoral immune response. Lymphocytes release antibodies into the bloodstream. These antibodies lower infection through three main pathways: neutralization, opsonization, and complement activation. Antibodies neutralize pathogens by binding to surface adhering proteins, keeping pathogens from binding to host cells. In opsonization, antibodies bind to the pathogen and create a target for phagocytic immune cells to find and latch onto, allowing them to destroy the pathogen more easily. Finally antibodies can also activate complement molecules which can combine in various ways to promote opsonization or even act directly to lyse a bacteria. There are many different kinds of antibody and their production is highly complex, involving several types of lymphocyte, but in general lymphocytes and other antibody regulating and producing cells will migrate to the lymph nodes to aid in the release of these antibodies into the bloodstream.[18]

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.

On the other side of things, there are natural killer cells; these cells are equipped with the heavy artillery needed to take down larger in size threats like bacteria, parasites, and tumor cells. A separate study[19] found that cortisol effectively disarmed natural killer cells, downregulating the expression of their natural cytotoxicity receptors. Interestingly, prolactin has the opposite effect. It increases the expression of cytotoxicity receptors on natural killer cells, increasing their firepower.

Cortisol stimulates many copper enzymes (often to 50% of their total potential), including lysyl oxidase, an enzyme that cross-links collagen and elastin. Especially valuable for immune response is cortisol's stimulation of the superoxide dismutase,[20] since this copper enzyme is almost certainly used by the body to permit superoxides to poison bacteria.

Cortisol counteracts insulin, contributes to hyperglycemia by stimulating gluconeogenesis[21] and inhibits the peripheral use of glucose (insulin resistance)[21][bettersourceneeded] by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane.[22] Cortisol also increases glycogen synthesis (glycogenesis) in the liver, storing glucose in easily accessible form.[23] 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.

Cortisol reduces bone formation,[4] favoring long-term development of osteoporosis (progressive bone disease). The mechanism behind this is two-fold: cortisol stimulates the production of RANKL by osteoblasts which stimulates, through binding to RANK receptors, the activity of osteoclasts cells responsible for calcium resorption from bone and also inhibits the production of osteoprotegerin (OPG) which acts as a decoy receptor and captures some RANKL before it can activate the osteoclasts through RANK.[7] In other words, when RANKL binds to OPG, no response occurs as opposed to the binding to RANK which leads to the activation of osteoclasts.

It transports potassium out of cells in exchange for an equal number of sodium ions (see above).[24] This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine.[25] Cortisol down-regulates the synthesis of collagen.[26]

Cortisol raises the free amino acids in the serum by inhibiting collagen formation, decreasing amino acid uptake by muscle, and inhibiting protein synthesis.[27] Cortisol (as opticortinol) may inversely inhibit IgA precursor cells in the intestines of calves.[28] Cortisol also inhibits IgA in serum, as it does IgM; however, it is not shown to inhibit IgE.[29]

Cortisol decreases glomerular filtration rate,[medical citation needed] and renal plasma flow from the kidneys thus increasing phosphate excretion,[medical citation needed] as well as increasing sodium and water retention and potassium excretion by acting on mineralocorticoid receptors. It also increases sodium and water absorption and potassium excretion in the intestines.[30]

Cortisol promotes sodium absorption through the small intestine of mammals.[31] Sodium depletion, however, does not affect cortisol levels[32] 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.[33]

A sodium load augments the intense potassium excretion by cortisol. Corticosterone is comparable to cortisol in this case.[34] For potassium to move out of the cell, cortisol moves an equal number of sodium ions into the cell.[24] 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 outcloser to the deoxycorticosterone effect).

Cortisol stimulates gastric-acid secretion.[35] 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.[36]

Cortisol works with adrenaline (epinephrine) 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.[37] However, long-term exposure to cortisol damages cells in the hippocampus;[38] this damage results in impaired learning.

Diurnal cycles of cortisol levels are found in humans.[8]

Sustained stress can lead to high levels of circulating cortisol (regarded as one of the more important of the several "stress hormones").[39]

During human pregnancy, increased fetal production of cortisol between weeks 30 and 32 initiates production of fetal lung pulmonary 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 were 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]

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 and other glucocorticoids, mineralocorticoid aldosterone, and dehydroepiandrosterone.[47]

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 sample type (blood or urine), 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.[medical citation needed]

Using the molecular weight of 362.460g/mole, the conversion factor from g/dL to nmol/L is approximately 27.6; thus, 10g/dL is about 276 nmol/L.[medical citation needed]

Cortisol follows a circadian rhythm, and to accurately measure cortisol levels is best to test four times per day through saliva. An individual may have normal total cortisol but have a lower than normal level during a certain period of the day and a higher than normal level during a different period. Therefore, some scholars question the clinical utility of cortisol measurement.[54][55][56][57]

Cortisol is lipophilic, and is transported bound to transcortin (also known as corticosteroid-binding globulin) and albumin, while only a small part of the total serum cortisol is unbound and has biological activity.[58] This binding to the corticosteroid-binding globulin is accomplished through hydrophobic interactions in which cortisol binds in a 1:1 ratio.[59] Serum cortisol assays measures total cortisol, and its results may be misleading for patients with altered serum protein concentrations. The salivary cortisol test avoids this problem because only free cortisol can pass through the salivary barrier.[medical citation needed] Transcortin particles are too large to pass through this barrier.[medical citation needed]

Automated immunoassays lack specificity and show significant cross-reactivity due to interactions with structural analogs of cortisol, and show differences between assays. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) can improve specificity and sensitivity.[60]

Some medical disorders are related to abnormal cortisol production, such as:

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.[64] 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.[65] (In swine, which do not produce arginine vasopressin, lysine vasopressin acts synergistically with CRH.[66])

When activated macrophages start to secrete IL-1, which synergistically with CRH increases ACTH,[16] 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.[67] 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.[68] 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[16]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,[67] 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.[69]

High-potassium media (which stimulates aldosterone secretion in vitro) also stimulate cortisol secretion from the fasciculata zone of canine adrenals[70][71] unlike corticosterone, upon which potassium has no effect.[72]

Potassium loading also increases ACTH and cortisol in humans.[73] 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.[74] This may also have a role in rheumatoid-arthritis pain; cell potassium is always low in RA.[75]

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 levels after treatment with ascorbic acid.[76]

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[84] or exceed[8] 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).[85]

Cortisol is metabolized reversibly to cortisone[86] by the 11-beta hydroxysteroid dehydrogenase system (11-beta HSD), which consists of two enzymes: 11-beta HSD1 and 11-beta HSD2. The metabolism of cortisol to cortisone involves oxidation of the hydroxyl group at the 11-beta position.[87]

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. If hexose-6-phosphate dehydrogenase (H6PDH) is present, the equilibrium can favor the activity of 11-beta HSD1. H6PDH regenerates NADPH, which increases the activity of 11-beta HSD1, and decreases the activity of 11-beta HSD2.[88]

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.[89]

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 also metabolized irreversibly 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.

Cortisol is also metabolized irreversibly into 6-hydroxycortisol by cytochrome p450-3A monooxygenases, mainly, CYP3A4.[90][91][86][92] Drugs that induce CYP3A4 may accelerate cortisol clearance.[93]

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

In animals, cortisol is often used as an indicator of stress and can be measured in blood,[94] saliva,[94] urine,[95] hair,[96] and faeces.[96][97]

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Cortisol - Wikipedia

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Growth hormone deficiency (GHD) is a rare condition in which the body does not make enough growth hormone (GH). Human growth hormone (GH) is a substance that controls childrens growth. Among children with short stature, GHD happens in approximately 1:4,000 to 1:10,000 cases.

GH is made by the pituitary gland, a small organ at the base of the brain. In children, GH is essential for normal growth, muscle and bone strength, and distribution of body fat. It also helps control glucose (sugar) and lipid (fat) levels in the body. Without enough GH, a child is likely to grow slowly and be much shorter than other children of the same age and gender.

GH works through a growth factor called insulin-like growth factor 1 (IGF-1). GH stimulates the liver to produce IGF-1 and release it into the circulation. IGF-1 then works at multiple tissues, like bone and cartilage, to promote growth. In addition, GH produces IGF-1 locally at tissues such as bone and cartilage.

Some children are born with GHD (congenital), while others develop it after birth (acquired).Children with congenital GHD may lack additional hormones produced by the pituitary gland.Some children with congenital GHD are found to have mutations (errors in the genes) that involve the development of the pituitary gland or GH production and action.In certain instances, congenital GH deficiency also can be seen as part of a syndrome that may affect the development of the middle of the face.

GHD may develop during childhood or adulthood (acquired GHD) after any process that can damage the pituitary gland or the surrounding brain area. Causes of acquired GHD include brain tumor, surgery, severe brain injury, or radiation of the area that is usually given for treatment of cancer. Rarely, acquired GHD can be the result of a chronic inflammation of the pituitary called hypophysitis, a condition that can be seen after treatment with certain cancer medications. In all these cases, the individual may have additional deficiencies of other pituitary hormones.

Most children with childhood-onset GHD have no additional hormone deficiencies, and doctors cannot find any cause for GHD. These cases of acquired GHD are also called isolated or idiopathic and are not inherited.For some children, slow growth is not caused by GHD.There are many reasons for slow growth and below-average height in children. At times, slow growth is normal and temporary, such as right before puberty starts. A pediatric endocrinologist (childrens hormone specialist) or primary care doctor can help find out why a child is growing slowly. Most children with GHD grow less than two inches (5 centimeters) each year.

The single most important clinical sign of GHD in children is growth failure. Children with GHD have severe short stature with normal proportions and appropriate body weight. Review of their growth chart usually shows a drop in height across two or more percentiles.

Your doctor will review your childs medical history and growth charts and look for signs of GHD and other conditions that affect growth. Your doctor may do tests to help find the cause of slow growth. These include:

X-Ray: An X-ray of the hand and wrist, called bone ageto assess growth potential in children.

Blood Tests: A doctor may order a blood test to rule out other conditions that affect growth.

IGF-1 levels: Additional blood work testing for levels of growth factors, such as Insulin-like growth factor (IGF-1) and insulin-like growth factor binding protein-3 (IGFBP-3), are helpful in diagnosing GHD.

GH stimulation test: During this test, the child is given medicines that stimulate the pituitary to release GH. If GH levels in the blood dont rise to a certain level, it can mean that the pituitary is not making enough GH.

Magnetic resonance image (MRI): An MRI (imaging test) of the head is usually done in individuals with GHD to look for a problem with the pituitary or the brain.

If IGF1 levels are low in the blood test, it may indicate that the person may have GHD. However, there are additional causes of low IGF1 levels, such as liver disease or low body weight.

Common symptoms that are present with a diagnosis of growth hormone deficiency include:

Babies with severe congenital GHD usually have only a slightly reduced birth length and may not immediately show signs of slow growth. In these children, a low blood sugar can be the main sign of GHD.

Adults with severe GHD may also experience:

Irradiation, surgery or injury to the pituitary area of the brain can increase the chance of developing acquired GHD. Untreated children with GHD reach a short adult height. Untreated GHD in adults may increase risk for heart disease and fractures.

People with GHD receive treatment with daily injections of synthetic (manufactured) human GH, a prescription medicine. GH is given at home as an injection under the skin at bedtime. More recently, a sustained release GH that is given as a weekly injection under the skin has become available.

Individuals treated with GH need regular doctor check-ups. In children, your doctor usually monitors the growth response to GH and changes in IGF1 levels in the blood and bone age x ray.

GH therapy is effective in improving growth and results in a normal adult height. The best results occur when GHD is diagnosed and treated early. In some children, GH can lead to four inches (10 centimeters) of growth during the first year of treatment. Therapy can continue until the child completes his/her growth and reaches adult height. At that point, the individual can be re-tested to see if he/she should continue GH therapy as an adult. Most of the childhood-onset cases of isolated GHD do not need therapy in adult life.In children, mild to moderate side effects are uncommon. They include:

Rare but serious side effects include:

For most children, the benefits of taking GH outweigh the risks.In adults, the GH side effects are also rare and can be swelling of hands and feet, joint pains and carpal tunnel syndrome. An increase risk for type II diabetes can happen in people with certain genetic predisposition such as Prader Will syndrome.

Concerns have been raised about a possibility that GH may increase an individuals cancer risk. Several studies so far point out that GH treatment for individuals with GHD does not increase the risk for leukemia or other cancers compared with age-matched healthy people.

You can help your child get the best care for GHD by taking these steps:

Endocrine Library >>

Editor(s): Alan Rogol, M.D., Henry Anhalt, DO, Melanie Schorr Haines, M.D., Maria George Vogiatzi, M.D.

Last Updated: January 24, 2022

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Growth Hormone Deficiency | Endocrine Society

Not what you're looking for? Overview

Even after we stop growing, adults still need growth hormone. Growth hormone is a protein made by the pituitary gland and released into the blood.

Growth hormone plays a role in healthy muscle, how our bodies collect fat (especially around the stomach area), the ratio of high density to low density lipoproteins in our cholesterol levels and bone density. In addition, growth hormone is needed for normal brain function.

A person who has too little adult growth hormone will have symptoms that include:

People with adult growth hormone deficiency have higher than normal levels of low-density lipoproteins in comparison to their high density lipoproteins. They also tend to have higher triglyceride levels. (Triglycerides are another type of fat that circulates in the blood and contributes to blocked blood vessels.)

A lack of growth hormone is usually caused by damage to the pituitary gland or the hypothalamus, a part of the brain that controls the pituitary gland. The damage may be due to a tumor; to surgery or radiation used to treat the tumor; or to problems with the blood supply to the pituitary gland.

In some cases, the lack of growth hormone is due to an injury to the pituitary gland.

A lack of growth hormone can appear either in childhood or in adulthood.

If a person has had surgery, an injury or a history of pituitary disorders, a doctor or endocrinologist (a specially trained physician who focuses on the health of hormone-secreting glands) will check for adult growth hormone deficiency. If there is a known disorder or problem with the pituitary gland, the doctor will probably order a magnetic resonance imaging (MRI) scan before any treatment is done. This allows the doctor to more accurately monitor how treatment is affecting the tumor.

Growth hormone in adults is absorbed quickly by tissues from the blood as it circulates. As a result of this, a blood test given to a healthy persons will show low levels of growth hormone. Endocrinologists instead check the pituitary gland's response when it is stimulated to produce growth hormone. These growth hormone stimulation tests are done in an outpatient setting and take about two to three hours. You will be asked not to eat before the test.

Once adult growth hormone deficiency has been confirmed, the doctor will prescribe daily doses of growth hormones. The hormone is injected into the patient's body; this can be done either by the patient or by a member of his or her family. Every four to eight weeks, the patient will return to the doctor for monitoring and a blood test to help the doctor decided if more hormone is needed or less.

If the person is getting too much growth hormone, he or she will have muscle or joint pain, swelling (fluid retention) and pain or numbness in the hands from carpal tunnel syndrome. If such symptoms appear, the doctor will lower the amount of growth hormone being given.

If the deficiency of growth hormone is due to a pituitary tumor, the doctor will monitor the tumor with MRIs every year. Currently, it is not known whether the growth hormone will cause tumors that remain in the pituitary gland to grow.

Finally, blood cholesterol and bone density will be monitored. With treatment of adult growth hormone deficiency, both of these measures should show signs of improvement.

Growth hormone therapy should not be given to people who have active cancer or tumors. It also should not be given to people who are seriously ill as a result of complications from open heart or abdominal surgery, who have multiple injuries from a major accident or who are have breathing problems. Taking growth hormone will not cause an adult to begin growing again.

Taking growth hormone can affect the way the body uses insulin, so it is important for anyone who has diabetes to keep their doctors informed and to be vigilant about monitoring blood sugar levels.

2000-2022 The StayWell Company, LLC. All rights reserved. This information is not intended as a substitute for professional medical care. Always follow your healthcare professional's instructions.

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Adult Growth Hormone Deficiency | Cedars-Sinai

Summary

growth hormone (GH), also called somatotropin or human growth hormone, peptide hormone secreted by the anterior lobe of the pituitary gland. It stimulates the growth of essentially all tissues of the body, including bone. GH is synthesized and secreted by anterior pituitary cells called somatotrophs, which release between one and two milligrams of the hormone each day. GH is vital for normal physical growth in children; its levels rise progressively during childhood and peak during the growth spurt that occurs in puberty.

In biochemical terms, GH stimulates protein synthesis and increases fat breakdown to provide the energy necessary for tissue growth. It also antagonizes (opposes) the action of insulin. GH may act directly on tissues, but much of its effect is mediated by stimulation of the liver and other tissues to produce and release insulin-like growth factors, primarily insulin-like growth factor 1 (IGF-1; formerly called somatomedin). The term insulin-like growth factor is derived from the ability of high concentrations of these factors to mimic the action of insulin, although their primary action is to stimulate growth. Serum IGF-1 concentrations increase progressively with age in children, with an accelerated increase at the time of the pubertal growth spurt. After puberty the concentrations of IGF-1 gradually decrease with age, as do GH concentrations.

GH secretion is stimulated by growth hormone-releasing hormone (GHRH) and is inhibited by somatostatin. In addition, GH secretion is pulsatile, with surges in secretion occurring after the onset of deep sleep that are especially prominent at the time of puberty. In normal subjects, GH secretion increases in response to decreased food intake and to physiological stresses and decreases in response to food ingestion. However, some individuals are affected by abnormalities in GH secretion, which involve either deficiency or overabundance of the hormone.

GH deficiency is one of the many causes of short stature and dwarfism. It results primarily from damage to the hypothalamus or to the pituitary gland during fetal development (congenital GH deficiency) or following birth (acquired GH deficiency). GH deficiency may also be caused by mutations in genes that regulate its synthesis and secretion. Affected genes include PIT-1 (pituitary-specific transcription factor-1) and POUF-1 (prophet of PIT-1). Mutations in these genes may also cause decreased synthesis and secretion of other pituitary hormones. In some cases, GH deficiency is the result of GHRH deficiency, in which case GH secretion may be stimulated by infusion of GHRH. In other cases, the somatotrophs themselves are incapable of producing GH, or the hormone itself is structurally abnormal and has little growth-promoting activity. In addition, short stature and GH deficiency are often found in children diagnosed with psychosocial dwarfism, which results from severe emotional deprivation. When children with this disorder are removed from the stressing, nonnurturing environment, their endocrine function and growth rate normalize.

Children with isolated GH deficiency are normal in size at birth, but growth retardation becomes evident within the first two years of life. Radiographs (X-ray films) of the epiphyses (the growing ends) of bones show growth retardation in relation to the patients chronological age. Although puberty is often delayed, fertility and delivery of normal children is possible in affected women.

GH deficiency is most often treated with injections of GH. For decades, however, availability of the hormone was limited, because it was obtained solely from human cadaver pituitaries. In 1985, use of natural GH was halted in the United States and several other countries because of the possibility that the hormone was contaminated with a type of pathogenic agent known as a prion, which causes a fatal condition called Creutzfeldt-Jakob disease. That same year, by means of recombinant DNA technology, scientists were able to produce a biosynthetic human form, which they called somatrem, thus assuring a virtually unlimited supply of this once-precious substance.

Children with GH deficiency respond well to injections of recombinant GH, often achieving near-normal height. However, some children, primarily those with the hereditary inability to synthesize GH, develop antibodies in response to injections of the hormone. Children with short stature not associated with GH deficiency may also grow in response to hormone injections, although large doses are often required.

A rare form of short stature is caused by an inherited insensitivity to the action of GH. This disorder is known as Laron dwarfism and is characterized by abnormal GH receptors, resulting in decreased GH-stimulated production of IGF-1 and poor growth. Serum GH concentrations are high because of the absence of the inhibitory action of IGF-1 on GH secretion. Dwarfism may also be caused by insensitivity of bone tissue and other tissues to IGF-1, resulting from decreased function of IGF-1 receptors.

GH deficiency often persists into adulthood, although some people affected in childhood have normal GH secretion in adulthood. GH deficiency in adults is associated with fatigue, decreased energy, depressed mood, decreased muscle strength, decreased muscle mass, thin and dry skin, increased adipose tissue, and decreased bone density. Treatment with GH reverses some of these abnormalities but can cause fluid retention, diabetes mellitus, and high blood pressure (hypertension).

Excess GH production is most often caused by a benign tumour (adenoma) of the somatotroph cells of the pituitary gland. In some cases, a tumour of the lung or of the pancreatic islets of Langerhans produces GHRH, which stimulates the somatotrophs to produce large amounts of GH. In rare cases, ectopic production of GH (production by tumour cells in tissues that do not ordinarily synthesize GH) causes an excess of the hormone. Somatotroph tumours in children are very rare and cause excessive growth that may lead to extreme height (gigantism) and features of acromegaly.

Acromegaly refers to the enlargement of the distal (acral) parts of the body, including the hands, feet, chin, and nose. The enlargement is due to the overgrowth of cartilage, muscle, subcutaneous tissue, and skin. Thus, patients with acromegaly have a prominent jaw, a large nose, and large hands and feet, as well as enlargement of most other tissues, including the tongue, heart, liver, and kidneys. In addition to the effects of excess GH, a pituitary tumour itself can cause severe headaches, and pressure of the tumour on the optic chiasm can cause visual defects.

Because the metabolic actions of GH are antagonistic (opposite) to those of insulin, some patients with acromegaly develop diabetes mellitus. Other problems associated with acromegaly include high blood pressure (hypertension), cardiovascular disease, and arthritis. Patients with acromegaly also have an increased risk of developing malignant tumours of the large intestine. Some somatotroph tumours also produce prolactin, which may cause abnormal lactation (galactorrhea). Patients with acromegaly are usually treated by surgical resection of the pituitary tumour. They can also be treated with radiation therapy or with drugs such as pegvisomant, which blocks the binding of growth hormone to its receptors, and synthetic long-acting analogues of somatostatin, which inhibit the secretion of GH.

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Growth hormone | Definition, Function, Deficiency, & Excess

A growth hormone deficiency (GHD) occurs when the pituitary gland doesnt produce enough growth hormone. It affects children more often than adults.

The pituitary gland is a small gland about the size of a pea. Its located at the base of the skull and secretes eight hormones. Some of these hormones control thyroid activity and body temperature.

GHD occurs in roughly 1 out of 7,000 births. The condition is also a symptom of several genetic diseases, including Prader-Willi syndrome.

You may be concerned that your child isnt meeting height and weight growth standards. But if its GHD, its important to know that its treatable. Children who are diagnosed early often recover very well. If left untreated, the condition can result in shorter-than-average height and delayed puberty.

Your body still needs growth hormone after youve finished puberty. Once youre in adulthood, the growth hormone maintains your body structure and metabolism. Adults can also develop GHD, but it isnt as common.

GHD that isnt present at birth may be caused by a tumor in the brain. These tumors are normally located at the site of the pituitary gland or the nearby hypothalamus region of the brain.

In children and adults, serious head injuries, infections, and radiation treatments can also cause GHD. This is called acquired growth hormone deficiency (AGHD).

Most cases of GHD are idiopathic, meaning that no cause has yet been found.

Children with GHD are shorter than their peers and have younger-looking, rounder faces. They may also have baby fat around the abdomen, even though their body proportions are average.

If GHD develops later in a childs life, such as from a brain injury or tumor, its main symptom is delayed puberty. In some instances, sexual development is halted.

Many teens with GHD experience low self-esteem due to developmental delays, such as short stature or a slow rate of maturing. For example, young women may not develop breasts and young mens voices may not change at the same rate as their peers.

Reduced bone strength is another symptom of AGHD. This may lead to more frequent fractures, especially in older adults.

People with low growth hormone levels may feel tired and lack stamina. They may experience sensitivity to hot or cold temperatures.

Those with GHD may experience certain psychological effects, including:

Adults with AGHD typically have high levels of fat in the blood and high cholesterol. This isnt due to poor diet, but rather to changes in the bodys metabolism caused by low levels of growth hormone. Adults with AGHD are at greater risk for diabetes and heart disease.

Your childs doctor will look for signs of GHD if your child isnt meeting their height and weight milestones. Theyll ask you about your growth rate as you approached puberty, as well as your other childrens growth rates. If they suspect GHD, a number of tests can confirm the diagnosis.

Your levels of growth hormone fluctuate widely throughout the day and night (diurnal variation). A blood test with a lower-than-normal result isnt enough evidence in itself to make a diagnosis.

One blood test can measure levels of proteins which are markers of growth hormone function but are much more stable. These are IGF-1 (insulin-like growth factor 1) and IGFPB-3 (insulin-like growth factor binding protein 3).

Your doctor may then go on to a GH stimulation test, if screening tests suggest that you have a GH deficiency.

Growth plates are the developing tissue at each end of your arm and leg bones. Growth plates fuse together when youve finished developing. X-rays of your childs hand can indicate their level of bone growth.

If a childs bone age is younger than their chronological age, this might be due to GHD.

If your doctor suspects a tumor or other damage to the pituitary gland, an MRI imaging scan can provide a detailed look inside the brain. Growth hormone levels will often be screened in adults who have a history of pituitary disorders, a brain injury, or who need brain surgery.

Testing can determine whether the pituitary condition was present at birth or brought on by an injury or tumor.

Since the mid-1980s, synthetic growth hormones have been used with great success to treat children and adults. Before synthetic growth hormones, natural growth hormones from cadavers were used for treatment.

Growth hormone is given by injection, typically into the bodys fatty tissues, such as the back of the arms, thighs, or buttocks. Its most effective as a daily treatment.

Side effects are generally minor, but may include:

In rare cases, long-term growth hormone injections may contribute to the development of diabetes, especially in people with a family history of that disease.

Children with congenital GHD are often treated with growth hormone until they reach puberty. Often, children who have too little growth hormone in their youth will naturally begin to produce enough as they enter adulthood.

However, some remain in treatment for their entire lives. Your doctor can determine whether you need ongoing injections by monitoring hormone levels in your blood.

Make an appointment with your doctor if you suspect that you or your child is deficient in growth hormones.

Many people respond very well to treatment. The sooner you start treatment, the better your results will be.

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Growth Hormone Deficiency: Causes, Symptoms & Diagnosis - Healthline

Chemical compounds that regulate plant growth and development

Plant hormone (or phytohormones) are signal molecules, produced within plants, that occur in extremely low concentrations. Plant hormones control all aspects of plant growth and development, from embryogenesis,[1] the regulation of organ size, pathogen defense,[2][3] stress tolerance[4][5] and through to reproductive development.[6] Unlike in animals (in which hormone production is restricted to specialized glands) each plant cell is capable of producing hormones.[7][8] Went and Thimann coined the term "phytohormone" and used it in the title of their 1937 book.[9]

Phytohormones occur across the plant kingdom, and even in algae, where they have similar functions to those seen in higher plants.[10] Some phytohormones also occur in microorganisms, such as unicellular fungi and bacteria, however in these cases they do not play a hormonal role and can better be regarded as secondary metabolites.[11]

The word hormone is derived from Greek, meaning set in motion. Plant hormones affect gene expression and transcription levels, cellular division, and growth. They are naturally produced within plants, though very similar chemicals are produced by fungi and bacteria that can also affect plant growth.[12] A large number of related chemical compounds are synthesized by humans. They are used to regulate the growth of cultivated plants, weeds, and in vitro-grown plants and plant cells; these manmade compounds are called plant growth regulators (PGRs). Early in the study of plant hormones, "phytohormone" was the commonly used term, but its use is less widely applied now.

Plant hormones are not nutrients, but chemicals that in small amounts promote and influence the growth,[13] development, and differentiation of cells and tissues. The biosynthesis of plant hormones within plant tissues is often diffuse and not always localized. Plants lack glands to produce and store hormones, because, unlike animalswhich have two circulatory systems (lymphatic and cardiovascular) powered by a heart that moves fluids around the bodyplants use more passive means to move chemicals around their bodies. Plants utilize simple chemicals as hormones, which move more easily through their tissues. They are often produced and used on a local basis within the plant body. Plant cells produce hormones that affect even different regions of the cell producing the hormone.

Hormones are transported within the plant by utilizing four types of movements. For localized movement, cytoplasmic streaming within cells and slow diffusion of ions and molecules between cells are utilized. Vascular tissues are used to move hormones from one part of the plant to another; these include sieve tubes or phloem that move sugars from the leaves to the roots and flowers, and xylem that moves water and mineral solutes from the roots to the foliage.

Not all plant cells respond to hormones, but those cells that do are programmed to respond at specific points in their growth cycle. The greatest effects occur at specific stages during the cell's life, with diminished effects occurring before or after this period. Plants need hormones at very specific times during plant growth and at specific locations. They also need to disengage the effects that hormones have when they are no longer needed. The production of hormones occurs very often at sites of active growth within the meristems, before cells have fully differentiated. After production, they are sometimes moved to other parts of the plant, where they cause an immediate effect; or they can be stored in cells to be released later. Plants use different pathways to regulate internal hormone quantities and moderate their effects; they can regulate the amount of chemicals used to biosynthesize hormones. They can store them in cells, inactivate them, or cannibalise already-formed hormones by conjugating them with carbohydrates, amino acids, or peptides. Plants can also break down hormones chemically, effectively destroying them. Plant hormones frequently regulate the concentrations of other plant hormones.[14] Plants also move hormones around the plant diluting their concentrations.

The concentration of hormones required for plant responses are very low (106 to 105 mol/L). Because of these low concentrations, it has been very difficult to study plant hormones, and only since the late 1970s have scientists been able to start piecing together their effects and relationships to plant physiology.[15] Much of the early work on plant hormones involved studying plants that were genetically deficient in one or involved the use of tissue-cultured plants grown in vitro that were subjected to differing ratios of hormones, and the resultant growth compared. The earliest scientific observation and study dates to the 1880s; the determination and observation of plant hormones and their identification was spread out over the next 70 years.

Different hormones can be sorted into different classes, depending on their chemical structures. Within each class of hormone, chemical structures can vary, but all members of the same class have similar physiological effects. Initial research into plant hormones identified five major classes: abscisic acid, auxins, brassinosteroids, cytokinins and ethylene.[16] This list was later expanded, and brassinosteroids, jasmonates, salicylic acid, and strigolactones are now also considered major plant hormones. Additionally there are several other compounds that serve functions similar to the major hormones, but their status as bona fide hormones is still debated.

Abscisic acid (also called ABA) is one of the most important plant growth inhibitors. It was discovered and researched under two different names, dormin and abscicin II, before its chemical properties were fully known. Once it was determined that the two compounds are the same, it was named abscisic acid. The name refers to the fact that it is found in high concentrations in newly abscissed or freshly fallen leaves.

This class of PGR is composed of one chemical compound normally produced in the leaves of plants, originating from chloroplasts, especially when plants are under stress. In general, it acts as an inhibitory chemical compound that affects bud growth, and seed and bud dormancy. It mediates changes within the apical meristem, causing bud dormancy and the alteration of the last set of leaves into protective bud covers. Since it was found in freshly abscissed leaves, it was initially thought to play a role in the processes of natural leaf drop, but further research has disproven this. In plant species from temperate parts of the world, abscisic acid plays a role in leaf and seed dormancy by inhibiting growth, but, as it is dissipated from seeds or buds, growth begins. In other plants, as ABA levels decrease, growth then commences as gibberellin levels increase. Without ABA, buds and seeds would start to grow during warm periods in winter and would be killed when it froze again. Since ABA dissipates slowly from the tissues and its effects take time to be offset by other plant hormones, there is a delay in physiological pathways that provides some protection from premature growth. Abscisic acid accumulates within seeds during fruit maturation, preventing seed germination within the fruit or before winter. Abscisic acid's effects are degraded within plant tissues during cold temperatures or by its removal by water washing in and out of the tissues, releasing the seeds and buds from dormancy.[17]

ABA exists in all parts of the plant, and its concentration within any tissue seems to mediate its effects and function as a hormone; its degradation, or more properly catabolism, within the plant affects metabolic reactions and cellular growth and production of other hormones.[18] Plants start life as a seed with high ABA levels. Just before the seed germinates, ABA levels decrease; during germination and early growth of the seedling, ABA levels decrease even more. As plants begin to produce shoots with fully functional leaves, ABA levels begin to increase again, slowing down cellular growth in more "mature" areas of the plant. Stress from water or predation affects ABA production and catabolism rates, mediating another cascade of effects that trigger specific responses from targeted cells. Scientists are still piecing together the complex interactions and effects of this and other phytohormones.

In plants under water stress, ABA plays a role in closing the stomata. Soon after plants are water-stressed and the roots are deficient in water, a signal moves up to the leaves, causing the formation of ABA precursors there, which then move to the roots. The roots then release ABA, which is translocated to the foliage through the vascular system[19] and modulates potassium and sodium uptake within the guard cells, which then lose turgidity, closing the stomata.[20][21]

Auxins are compounds that positively influence cell enlargement, bud formation, and root initiation. They also promote the production of other hormones and, in conjunction with cytokinins, control the growth of stems, roots, and fruits, and convert stems into flowers.[22] Auxins were the first class of growth regulators discovered.A Dutch Biologist Frits Warmolt Went first described auxins.[23] They affect cell elongation by altering cell wall plasticity. They stimulate cambium, a subtype of meristem cells, to divide, and in stems cause secondary xylem to differentiate.

Auxins act to inhibit the growth of buds lower down the stems in a phenomenon known as apical dominance, and also to promote lateral and adventitious root development and growth. Leaf abscission is initiated by the growing point of a plant ceasing to produce auxins. Auxins in seeds regulate specific protein synthesis,[24] as they develop within the flower after pollination, causing the flower to develop a fruit to contain the developing seeds.

In large concentrations, auxins are often toxic to plants; they are most toxic to dicots and less so to monocots. Because of this property, synthetic auxin herbicides including 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) have been developed and used for weed control by defoliation. Auxins, especially 1-naphthaleneacetic acid (NAA) and indole-3-butyric acid (IBA), are also commonly applied to stimulate root growth when taking cuttings of plants. The most common auxin found in plants is indole-3-acetic acid (IAA).

Brassinosteroids are a class of polyhydroxysteroids, the only example of steroid-based hormones in plants. Brassinosteroids control cell elongation and division, gravitropism, resistance to stress, and xylem differentiation. They inhibit root growth and leaf abscission. Brassinolide was the first identified brassinosteroid and was isolated from extracts of rapeseed (Brassica napus) pollen in 1979.[25] Brassinosteroids are a class of steroidal phytohormones in plants that regulate numerous physiological processes. This plant hormone was identified by Mitchell et al. who extracted ingredients from Brassica pollen only to find that the extracted ingredients main active component was Brassinolide.[26] This finding meant the discovery of a new class of plant hormones called Brassinosteroids. These hormones act very similarly to animal steroidal hormones by promoting growth and development. In plants these steroidal hormones play an important role in cell elongation via BR signaling.[27] Brassinosteroids receptor- brassinosteroid insensitive 1 (BRI1) is the main receptor for this signaling pathway. This BRI1 receptor was found by Clouse et al. who made the discovery by inhibiting BR and comparing it to the wildtype in Arabidopsis. The BRI1 mutant displayed several problems associated with growth and development such as dwarfism, reduced cell elongation and other physical alterations.[26] These findings mean that plants properly expressing brassinosteroids grow more than their mutant counterparts. Brassinosteroids bind to BRI1 localized at the plasma membrane[28] which leads to a signal cascade that further regulates cell elongation. This signal cascade however is not entirely understood at this time. What is believed to be happening is that BR binds to the BAK1 complex which leads to a phosphorylation cascade.[29] This phosphorylation cascade then causes BIN2 to be deactivated which causes the release of transcription factors.[29] These released transcription factors then bind to DNA that leads to growth and developmental processes [29] and allows plants to respond to abiotic stressors.[30]

Cytokinins or CKs are a group of chemicals that influence cell division and shoot formation. They also help delay senescence of tissues, are responsible for mediating auxin transport throughout the plant, and affect internodal length and leaf growth. They were called kinins in the past when they were first isolated from yeast cells. Cytokinins and auxins often work together, and the ratios of these two groups of plant hormones affect most major growth periods during a plant's lifetime. Cytokinins counter the apical dominance induced by auxins; in conjunction with ethylene, they promote abscission of leaves, flower parts, and fruits.[31]

Among the plant hormones, the 3 that are known to help with immunological interactions are ethylene (ET), salicylates (SA), and jasmonates (JA), however more research has gone into identifying the role that cytokinins (CK) play in this. Evidence suggests that cytokinins delay the interactions with pathogens, showing signs that they could induce resistance toward these pathogenic bacteria. Accordingly, there are higher CK levels in plants that have increased resistance to pathogens compared to those which are more susceptible.[32] For example, pathogen resistance involving cytokinins was tested using the Arabidopsis species by treating them with naturally occurring CK (trans-zeatin) to see their response to the bacteria Pseudomonas syringa. Tobacco studies reveal that over expression of CK inducing IPT genes yields increased resistance whereas over expression of CK oxidase yields increased susceptibility to pathogen, namely P. syringae.

While theres not much of a relationship between this hormone and physical plant behavior, there are behavioral changes that go on inside the plant in response to it. Cytokinin defense effects can include the establishment and growth of microbes (delay leaf senescence), reconfiguration of secondary metabolism or even induce the production of new organs such as galls or nodules.[33] These organs and their corresponding processes are all used to protect the plants against biotic/abiotic factors.

Unlike the other major plant hormones, ethylene is a gas and a very simple organic compound, consisting of just six atoms. It forms through the breakdown of methionine, an amino acid which is in all cells. Ethylene has very limited solubility in water and therefore does not accumulate within the cell, typically diffusing out of the cell and escaping the plant. Its effectiveness as a plant hormone is dependent on its rate of production versus its rate of escaping into the atmosphere. Ethylene is produced at a faster rate in rapidly growing and dividing cells, especially in darkness. New growth and newly germinated seedlings produce more ethylene than can escape the plant, which leads to elevated amounts of ethylene, inhibiting leaf expansion (see hyponastic response).

As the new shoot is exposed to light, reactions mediated by phytochrome in the plant's cells produce a signal for ethylene production to decrease, allowing leaf expansion. Ethylene affects cell growth and cell shape; when a growing shoot or root hits an obstacle while underground, ethylene production greatly increases, preventing cell elongation and causing the stem to swell. The resulting thicker stem is stronger and less likely to buckle under pressure as it presses against the object impeding its path to the surface. If the shoot does not reach the surface and the ethylene stimulus becomes prolonged, it affects the stem's natural geotropic response, which is to grow upright, allowing it to grow around an object. Studies seem to indicate that ethylene affects stem diameter and height: when stems of trees are subjected to wind, causing lateral stress, greater ethylene production occurs, resulting in thicker, sturdier tree trunks and branches.

Ethylene also affects fruit ripening. Normally, when the seeds are mature, ethylene production increases and builds up within the fruit, resulting in a climacteric event just before seed dispersal. The nuclear protein Ethylene Insensitive2 (EIN2) is regulated by ethylene production, and, in turn, regulates other hormones including ABA and stress hormones.[34] Ethylene diffusion out of plants is strongly inhibited underwater. This increases internal concentrations of the gas. In numerous aquatic and semi-aquatic species (e.g. Callitriche platycarpus, rice, and Rumex palustris), the accumulated ethylene strongly stimulates upward elongation. This response is an important mechanism for the adaptive escape from submergence that avoids asphyxiation by returning the shoot and leaves to contact with the air whilst allowing the release of entrapped ethylene.[35][36][37][38] At least one species (Potamogeton pectinatus)[39] has been found to be incapable of making ethylene while retaining a conventional morphology. This suggests ethylene is a true regulator rather than being a requirement for building a plant's basic body plan.

Gibberellins (GAs) include a large range of chemicals that are produced naturally within plants and by fungi. They were first discovered when Japanese researchers, including Eiichi Kurosawa, noticed a chemical produced by a fungus called Gibberella fujikuroi that produced abnormal growth in rice plants.[40] It was later discovered that GAs are also produced by the plants themselves and control multiple aspects of development across the life cycle. The synthesis of GA is strongly upregulated in seeds at germination and its presence is required for germination to occur. In seedlings and adults, GAs strongly promote cell elongation. GAs also promote the transition between vegetative and reproductive growth and are also required for pollen function during fertilization.[41]

Gibberellins breaks the dormancy (in active stage) in seeds and buds and helps increasing the height of the plant. It helps in the growth of the stem[citation needed]

Jasmonates (JAs) are lipid-based hormones that were originally isolated from jasmine oil.[42] JAs are especially important in the plant response to attack from herbivores and necrotrophic pathogens.[43] The most active JA in plants is jasmonic acid. Jasmonic acid can be further metabolized into methyl jasmonate (MeJA), which is a volatile organic compound. This unusual property means that MeJA can act as an airborne signal to communicate herbivore attack to other distant leaves within one plant and even as a signal to neighboring plants.[44] In addition to their role in defense, JAs are also believed to play roles in seed germination, the storage of protein in seeds, and root growth.[43]

JAs have been shown to interact in the signalling pathway of other hormones in a mechanism described as crosstalk. The hormone classes can have both negative and positive effects on each other's signal processes.[45]

Jasmonic acid methyl ester (JAME) has been shown to regulate genetic expression in plants.[46] They act in signalling pathways in response to herbivory, and upregulate expression of defense genes.[47] Jasmonyl-isoleucine (JA-Ile) accumulates in response to herbivory, which causes an upregulation in defense gene expression by freeing up transcription factors.[47]

Jasmonate mutants are more readily consumed by herbivores than wild type plants, indicating that JAs play an important role in the execution of plant defense. When herbivores are moved around leaves of wild type plants, they reach similar masses to herbivores that consume only mutant plants, implying the effects of JAs are localized to sites of herbivory.[48] Studies have shown that there is significant crosstalk between defense pathways.[49]

Salicylic acid (SA) is a hormone with a structure related to phenol. It was originally isolated from an extract of white willow bark (Salix alba) and is of great interest to human medicine, as it is the precursor of the painkiller aspirin. In plants, SA plays a critical role in the defense against biotrophic pathogens. In a similar manner to JA, SA can also become methylated. Like MeJA, methyl salicylate is volatile and can act as a long-distance signal to neighboring plants to warn of pathogen attack. In addition to its role in defense, SA is also involved in the response of plants to abiotic stress, particularly from drought, extreme temperatures, heavy metals, and osmotic stress.[50]

Salicylic acid (SA) serves as a key hormone in plant innate immunity, including resistance in both local and systemic tissue upon biotic attacks, hypersensitive responses, and cell death. Some of the SA influences on plants include seed germination, cell growth, respiration, stomatal closure, senescence-associated gene expression, responses to abiotic and biotic stresses, basal thermo tolerance and fruit yield. A possible role of salicylic acid in signaling disease resistance was first demonstrated by injecting leaves of resistant tobacco with SA.[51] The result was that injecting SA stimulated pathogenesis related (PR) protein accumulation and enhanced resistance to tobacco mosaic virus (TMV) infection. Exposure to pathogens causes a cascade of reactions in the plant cells. SA biosynthesis is increased via isochorismate synthase (ICS) and phenylalanine ammonia-lyase (PAL) pathway in plastids.[52] It was observed that during plant-microbe interactions, as part of the defense mechanisms, SA is initially accumulated at the local infected tissue and then spread all over the plant to induce systemic acquired resistance at non-infected distal parts of the plant. Therefore with increased internal concentration of SA, plants were able to build resistant barriers for pathogens and other adverse environmental conditions[53]

Strigolactones (SLs) were originally discovered through studies of the germination of the parasitic weed Striga lutea. It was found that the germination of Striga species was stimulated by the presence of a compound exuded by the roots of its host plant.[54] It was later shown that SLs that are exuded into the soil also promote the growth of symbiotic arbuscular mycorrhizal (AM) fungi.[55] More recently, another role of SLs was identified in the inhibition of shoot branching.[56] This discovery of the role of SLs in shoot branching led to a dramatic increase in the interest in these hormones, and it has since been shown that SLs play important roles in leaf senescence, phosphate starvation response, salt tolerance, and light signalling.[57]

Other identified plant growth regulators include:

Synthetic plant hormones or PGRs are used in a number of different techniques involving plant propagation from cuttings, grafting, micropropagation and tissue culture. Most commonly they are commercially available as "rooting hormone powder".

The propagation of plants by cuttings of fully developed leaves, stems, or roots is performed by gardeners utilizing auxin as a rooting compound applied to the cut surface; the auxins are taken into the plant and promote root initiation. In grafting, auxin promotes callus tissue formation, which joins the surfaces of the graft together. In micropropagation, different PGRs are used to promote multiplication and then rooting of new plantlets. In the tissue-culturing of plant cells, PGRs are used to produce callus growth, multiplication, and rooting.

Plant hormones affect seed germination and dormancy by acting on different parts of the seed.

Embryo dormancy is characterized by a high ABA:GA ratio, whereas the seed has high abscisic acid sensitivity and low GA sensitivity. In order to release the seed from this type of dormancy and initiate seed germination, an alteration in hormone biosynthesis and degradation toward a low ABA/GA ratio, along with a decrease in ABA sensitivity and an increase in GA sensitivity, must occur.

ABA controls embryo dormancy, and GA embryo germination.Seed coat dormancy involves the mechanical restriction of the seed coat. This, along with a low embryo growth potential, effectively produces seed dormancy. GA releases this dormancy by increasing the embryo growth potential, and/or weakening the seed coat so the radical of the seedling can break through the seed coat.Different types of seed coats can be made up of living or dead cells, and both types can be influenced by hormones; those composed of living cells are acted upon after seed formation, whereas the seed coats composed of dead cells can be influenced by hormones during the formation of the seed coat. ABA affects testa or seed coat growth characteristics, including thickness, and effects the GA-mediated embryo growth potential. These conditions and effects occur during the formation of the seed, often in response to environmental conditions. Hormones also mediate endosperm dormancy: Endosperm in most seeds is composed of living tissue that can actively respond to hormones generated by the embryo. The endosperm often acts as a barrier to seed germination, playing a part in seed coat dormancy or in the germination process. Living cells respond to and also affect the ABA:GA ratio, and mediate cellular sensitivity; GA thus increases the embryo growth potential and can promote endosperm weakening. GA also affects both ABA-independent and ABA-inhibiting processes within the endosperm.[66]

Willow bark has been used for centuries as a painkiller. The active ingredient in willow bark that provides these effects is the hormone salicylic acid (SA). In 1899, the pharmaceutical company Bayer began marketing a derivative of SA as the drug aspirin.[67] In addition to its use as a painkiller, SA is also used in topical treatments of several skin conditions, including acne, warts and psoriasis.[68] Another derivative of SA, sodium salicylate has been found to suppress proliferation of lymphoblastic leukemia, prostate, breast, and melanoma human cancer cells.[69]

Jasmonic acid (JA) can induce death in lymphoblastic leukemia cells. Methyl jasmonate (a derivative of JA, also found in plants) has been shown to inhibit proliferation in a number of cancer cell lines,[69] although there is still debate over its use as an anti-cancer drug, due to its potential negative effects on healthy cells.[70]

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Plant hormone - Wikipedia