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Aside from making healthy lifestyle choices and addressing medication side effects or untreated medical conditions, there's little you can do to naturally boost your testosterone level.

Testosterone levels vary greatly among men. In general, however, older men tend to have lower testosterone levels than do younger men. Testosterone levels gradually decline throughout adulthood about 1 percent a year after age 30 on average.

A blood test is the only way to diagnose a low testosterone level or a reduction in the bioavailability of testosterone. Some men have a lower than normal testosterone level without signs or symptoms. For most men, no treatment is needed. But for some others, very low testosterone levels lead to a condition in which bones become weak and brittle (osteoporosis). For others, low testosterone might cause changes in sexual function, sleep patterns, emotions and the body.

However, some of these signs and symptoms can be caused by factors other than low testosterone, including medication side effects, thyroid problems, depression and excessive alcohol use. There are also conditions, such as obstructive sleep apnea, that might affect testosterone levels. Once these conditions are identified and treated, testosterone typically will return to a normal level.

If you are experiencing signs and symptoms that might be the result of a low testosterone level, consult your doctor. He or she can evaluate possible causes for the way you feel and explain possible treatment options. In addition, these steps might help:

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Testosterone level: Can you boost it naturally? - Mayo Clinic

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Mar 20th, 2019 | Filed under Testosterone

What are androgens?

Hormones are chemical messengers madeby glands in the body that are carried inthe blood to act on other organs in thebody. Hormones are needed for growth,reproduction and well-being.

Androgens are male sex hormones thatincrease at puberty and are needed for aboy to develop into a sexually mature adultwho can reproduce. The most importantandrogen is testosterone.

Testosterone is the most important androgen (male sex hormone) in men and it is needed for normal reproductive and sexual function. Testosterone is important for the physical changes that happen during male puberty, such as development of the penis and testes, and for the features typical of adult men such as facial and body hair and a masculine physique. Testosterone also acts on cells in the testes to make sperm.

Testosterone is also important for overall good health. It helps the growth of bones and muscles, and affects mood and libido (sex drive). Some testosterone is changed into oestrogen, the female sex hormone, and this is important for bone health in men.

Testosterone is mainly made in the testes. A small amount of testosterone is also made by the adrenal glands, which are walnut-sized glands that sit on top of the kidneys.

The pituitary gland and the hypothalamus,located at the base of the brain, controlthe production of male hormones andsperm. Luteinizing hormone (LH) andfollicle stimulating hormone (FSH) arethe two important messenger hormonesmade by the pituitary gland that act onthe testes.

LH is needed for the Leydig cells in thetestes to make testosterone, the male sexhormone. Testosterone and FSH from thepituitary gland then act together on theseminiferous tubules (sperm-producingtubes) in the testes to make sperm.

Androgen, or testosterone, deficiency iswhen the body is not able to make enoughtestosterone for the body to functionnormally. Although not a life-threateningproblem, androgen deficiency can affectyour quality of life.

Androgen deficiency due to diseases of the testes or hypothalamus-pituitary affects about one in 200 men under 60 years of age. It is likely that androgen deficiency is under-diagnosed and that many men are missing out on the benefits of treatment. About one in 10 older men may have testosterone levels lower than those in young men, but this is usually linked with chronic illness and obesity. The benefits and risks of testosterone treatment for such men are not yet known.

Testosterone levels in men are highestbetween the ages of 20 and 30 years. Asmen age there is a small, gradual drop intestosterone levels; they may drop by up toone third between 30 and 80 years of age.

Some men will have a greater drop intestosterone levels as they age, especiallywhen they are obese or have other chronic(long-term) medical problems. On the otherhand, healthy older men with normal bodyweight may not experience any drop inserum testosterone levels.

There is no such thing as male menopauseor andropause that can be compared tomenopause in women.

Low energy levels, mood swings, irritability,poor concentration, reduced muscle strengthand low sex drive can be symptoms ofandrogen deficiency (low testosterone).Symptoms often overlap with those of otherillnesses. The symptoms of androgen deficiencyare different for men of different ages.

Androgen deficiency can be caused bygenetic disorders, medical problems, ordamage to the testes or pituitary gland.Androgen deficiency happens when thereare problems within the testes or withhormone production in the brain. A commonchromosomal disorder that causes androgendeficiency is Klinefelters syndrome.

A diagnosis of androgen deficiency involveshaving a thorough medical evaluation andat least two blood samples (taken in themorning on different days) to measurehormone levels. Diagnosis should not be simply based on symptoms as these could becaused by other health problems that needdifferent treatment. A diagnosis of androgendeficiency is only confirmed when blood testsshow a lower than normal testosterone level.

A reference range is used as a guide by testing laboratories and doctors to decide whether a persons hormone levels are normal or low, and whether treatment may be needed. Testosterone is measured in units called nanomalor. The normal testosterone reference range for healthy, young adult men is about 8 to 27 nanomolar but these numbers vary between measurement systems.

Androgen deficiency is treated with testosterone therapy; this means giving testosterone in doses that return the testosterone levels in the blood to normal. Testosterone is prescribed for men with androgen deficiency confirmed by blood tests. Once started, testosterone therapy is usually continued for life and the man needs to be checked regularly by a doctor.

In Australia testosterone therapy is available in the form of injections, gels, creams, patches and tablets, and works very well for men with confirmed androgen (testosterone) deficiency. The type of treatment prescribed can depend on patient convenience, familiarity and cost. Commercial testosterone products contain only the natural testosterone molecule that is chemically produced from plant materials.

Side-effects are not expected because testosterone therapy aims to bring a mans testosterone levels back to normal. However, testosterone therapy can increase the growth of the prostate gland which can make the symptoms of benign prostate enlargement (such as needing to urinate more often) worse. In the case of prostate cancer, testosterone therapy is not used because of concerns that it can make the tumour grow. Too high a dose of testosterone can lead to acne, weight gain, gynaecomastia (breast development), male-pattern hair loss and changes in mood. Any side-effects should be managed by a doctor and the testosterone dose lowered.

There are many herbal products marketed, particularly on the Internet, as treatmentsthat can act like testosterone and improve muscle strength and libido (sex drive). However, there are no known herbal products that can replace testosterone in the body and be used to treat androgen deficiency.

Testosterone therapy generally stops the production of the pituitary hormones FSH and LH, which reduces the size of the testes and can lower or stop sperm being made.

Testosterone treatment should not be given to a man wanting to become a father in the foreseeable future. If sperm production was normal before testosterone therapy, it usually recovers after treatment stops but it can take many months to go back to normal.

Testosterone therapy in men with androgen deficiency aims to bring testosterone levels back to normal and to return muscle strength and energy levels back to normal. However, the use of androgens (anabolic steroids) by normal men to improve athletic performance is illegal and has important short-term and long-term health risks.

Men who use anabolic steroids will lower or even turn off their own testosterone and sperm production. It may take many months for testosterone levels and sperm counts to return to normal after stopping anabolic steroids.

There are no known ways to prevent androgen deficiency caused by damage to the testes or pituitary gland. However, if you live a healthier lifestyle and manage other health problems your testosterone levels may improve, if your low testosterone levels are caused by other illness.

Not all men have a drop in testosterone levels with age. A healthy lifestyle may help you to keep testosterone levels normal.

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Mar 9th, 2019 | Filed under Testosterone

Progene is formulated to gradually supplement existing naturalprocesses. As a natural, non-synthetic solution, individual results will absolutely vary. Remember that not all supplements are for everyone. If you are taking other medications, drugs that require a prescription, have a medical condition, a history of heart conditions, issues with blood pressure regulation, or have prostate issues, ask your doctor if Progene is right for you. The information in this Website is provided for informational purposes only. It is not intended as and should not be relied upon as medical advice. Additional site terms apply Terms of use. The individuals shown may be renumerated models and depending on the page, may or may not be actual Progene customers or staff. The statements on this website have not been evaluated by the Food and Drug Administration. The FDA only evaluates foods and drugs, not supplements like these products. Progene is not intended to diagnose, treat, cure or prevent any disease. Testosterone loss due to natural aging is a natural process and not considered a medical condition.

2018 Progene HealthCare, Inc.Progene is a registered trademark of Progene HealthCare, Inc.All Rights Reserved.

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Feb 1st, 2019 | Filed under Testosterone

Alternative names for testosterone

Testo (brand name for testosterone formulations); 4-androsten-17-ol-3-one

Testosterone is produced by the gonads (by the Leydig cells in testes in men and by the ovaries in women), although small quantities are also produced by the adrenal glands in both sexes.It is an androgen, meaning that it stimulates the development of male characteristics.

Present in much greater levels in men than women, testosterone initiates the development of the male internal and external reproductive organs during foetal development and is essential for the production of sperm in adult life.This hormone also signals the body to make new blood cells, ensures that muscles and bones stay strong during and after puberty and enhances libido both in men and women.Testosterone is linked to many of the changes seen in boys during puberty (including an increase in height, body and pubic hair growth, enlargement of the penis, testes and prostate gland, and changes in sexual and aggressive behaviour).It also regulates the secretion of luteinising hormone and follicle stimulating hormone.To effect these changes, testosterone is often converted into another androgen called dihydrotestosterone.

In women, testosterone is produced by the ovaries and adrenal glands.The majority of testosterone produced in the ovary is converted to the principle female sex hormone, oestradiol.

The regulation of testosterone production is tightly controlled to maintain normal levels in blood, although levels are usually highest in the morning and fall after that.The hypothalamus and the pituitary gland are important in controlling the amount of testosterone produced by the testes.In response to gonadotrophin-releasing hormone from the hypothalamus, the pituitary gland produces luteinising hormone which travels in the bloodstream to the gonads and stimulates the production and release of testosterone.

As blood levels of testosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone.

The effect excess testosterone has on the body depends on both age and sex. It is unlikely that adult men will develop a disorder in which they produce too much testosterone and it is often difficult to spot that an adult male has too much testosterone.More obviously, young children with too much testosterone may enter a false growth spurt and show signs of early puberty and young girls may experience abnormal changes to their genitalia. In both males and females, too much testosterone can lead to precocious puberty and result in infertility.

In women, high blood levels of testosterone may also be an indicator of polycystic ovary syndrome.Women with this condition may notice increased acne, body and facial hair (called hirsutism), balding at the front of the hairline, increased muscle bulk and a deepening voice.

There are also several conditions that cause the body to produce too much testosterone.These include androgen resistance, congenital adrenal hyperplasia and ovarian cancer.

The use of anabolic steroids (manufactured androgenic hormones) shuts down the release of luteinising hormone and follicle stimulating hormone secretion from the pituitary gland, which in turn decreases the amount of testosterone and sperm produced within the testes. In men, prolonged exposure to anabolic steroids results in infertility, a decreased sex drive, shrinking of the testes and breast development. Liver damage may result from its prolonged attempts to detoxify the anabolic steroids.Behavioural changes (such as increased irritability) may also be observed.Undesirable reactions also occur in women who take anabolic steroids regularly, as a high concentration of testosterone, either natural or manufactured, can cause masculinisation (virilisation) of women.

If testosterone deficiency occurs during fetal development, then male characteristics may not completely develop. If testosterone deficiency occurs during puberty, a boys growth may slow and no growth spurt will be seen.The child may have reduced development of pubic hair, growth of the penis and testes, and deepening of the voice. Around the time of puberty, boys with too little testosterone may also have less than normal strength and endurance, and their arms and legs may continue to grow out of proportion with the rest of their body.

In adult men, low testosterone may lead to a reduction in muscle bulk, loss of body hair and a wrinkled parchment-like appearance of the skin. Testosterone levels in men decline naturally as they age. In the media, this is sometimes referred to as the male menopause (andropause).

Low testosterone levels can cause mood disturbances, increased body fat, loss of muscle tone, inadequate erections and poor sexual performance, osteoporosis, difficulty with concentration, memory loss and sleep difficulties. Current research suggests that this effect occurs in only a minority (about 2%) of ageing men.However, there is a lot of research currently in progress to find out more about the effects of testosterone in older men and also whether the use of testosterone replacement therapy would have any benefits.

Last reviewed: Feb 2018

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Dec 28th, 2018 | Filed under Testosterone

OxandroloneClinical dataTrade namesOxandrin, Anavar, othersSynonymsVar; CB-8075; NSC-67068; SC-11585; Protivar; 17-Methyl-2-oxa-4,5-dihydrotestosterone; 17-Methyl-2-oxa-DHT; 17-Methyl-2-oxa-5-androstan-17-ol-3-oneAHFS/Drugs.comMonographMedlinePlusa604024PregnancycategoryRoutes ofadministrationBy mouthDrug classAndrogen; Anabolic steroidATC codeLegal statusLegal statusPharmacokinetic dataBioavailability97%[2]Protein binding9497%[2]MetabolismKidneys (primarily), liver[1][2]Elimination half-lifeAdults: 9.410.4 hours[2][3]Elderly: 13.3 hours[3]ExcretionUrine: 28% (unchanged)[3]Feces: 3%[3]Identifiers

C[C@]12CC[C@H]3[C@H]([C@@H]1CC[C@]2(C)O)CC[C@@H]4[C@@]3(COC(=O)C4)C

Oxandrolone, sold under the brand names Oxandrin and Anavar, among others, is an androgen and anabolic steroid (AAS) medication which is used to help promote weight gain in various situations, to help offset protein catabolism caused by long-term corticosteroid therapy, to support recovery from severe burns, to treat bone pain associated with osteoporosis, to aid in the development of girls with Turner syndrome, and for other indications.[4][5][6] It is taken by mouth.[4]

Side effects of oxandrolone include symptoms of masculinization such as acne, increased hair growth, voice changes, and increased sexual desire.[4] Uniquely among most AAS that are active by mouth, it seems to have little risk of liver damage.[4][7] The drug is a synthetic androgen and anabolic steroid, hence is an agonist of the androgen receptor (AR), the biological target of androgens such as testosterone and dihydrotestosterone.[4][8] It has strong anabolic effects and weak androgenic effects, which give it a mild side effect profile and make it especially suitable for use in women.[4]

Oxandrolone was first described in 1962 and was introduced for medical use in 1964.[4] It is used mostly in the United States.[4][9] In addition to its medical use, oxandrolone is used to improve physique and performance.[4][10] The drug is a controlled substance in many countries, so nonmedical use is generally illicit.[4][11][12][13]

Oxandrolone has been researched and prescribed as a treatment for a wide variety of conditions. It is FDA-approved for treating bone pain associated with osteoporosis, aiding weight gain following surgery or physical trauma, during chronic infection, or in the context of unexplained weight loss, and counteracting the catabolic effect of long-term corticosteroid therapy.[14][15] As of 2016[update], it is often prescribed off-label to quicken recovery from severe burns, aid the development of girls with Turner syndrome, and counteract HIV/AIDS-induced wasting. Oxandrolone improves both short-term and long-term outcomes in people recovering from severe burns and is well-established as a safe treatment for this indication.[5][6] It is also used in the treatment of idiopathic short stature, anemia, hereditary angioedema, alcoholic hepatitis, and hypogonadism.[16][17]

Medical research has established the effectiveness of oxandrolone in aiding the development of girls with Turner syndrome. Although oxandrolone has long been used to accelerate growth in children with idiopathic short stature, it is unlikely to increase adult height, and in some cases may even decrease it. Oxandrolone has, therefore, largely been replaced by growth hormone for this use.[18] Children with idiopathic short stature or Turner syndrome are given doses of oxandrolone far smaller than those given to people with burns to minimize the likelihood of virilization and premature maturation.[18][19]

Many bodybuilders and athletes use oxandrolone for its muscle-building effects.[4] It is much more anabolic than androgenic, so women and those seeking less intense steroid regimens use it particularly often.[4] Many also value oxandrolone's low hepatotoxicity relative to most other orally active AASs.[4]

Like other AASs, oxandrolone may worsen hypercalcemia by increasing osteolytic bone resorption.[14] When taken by pregnant women, oxandrolone may have unintended effects such as masculinization on the fetus.[14]

Women who are administered oxandrolone may experience virilization, irreversible development of masculine features such as voice deepening, hirsutism, menstruation abnormalities, male-pattern hair loss, and clitoral enlargement.[18][14][19] Oxandrolone may disrupt growth in children, reducing their adult height.[20][bettersourceneeded] Because of these side effects, doses given to women and children are minimized and people are usually monitored for virilization and growth abnormalities.[18][19] Like other androgens, oxandrolone can cause or worsen acne and priapism (unwanted or prolonged erections).[14][20] Oxandrolone can also reduce males' fertility, another side effect common among androgens.[20] In an attempt to compensate for the exogenous increase in androgens, the body may reduce testosterone production via testicular atrophy and inhibition of gonadotropic activity.[14]

Unlike some AASs, oxandrolone does not generally cause gynecomastia because it is not aromatized into estrogenic metabolites.[21] However, although no reports of gynecomastia were made in spite of widespread use, oxandrolone was reported in a publication in 1991 to have been associated with 33cases of gynecomastia in adolescent boys treated with it for short stature.[22][23] The gynecomastia developed during oxandrolone therapy in 19 of the boys and after the therapy was completed in 14 of the boys, and 10 of the boys had transient gynecomastia, while 23 had persistent gynecomastia that necessitated mastectomy.[22][23] Though transient gynecomastia is a natural and common occurrence in pubertal boys, the gynecomastia associated with oxandrolone was of a late/delayed onset and was persistent in a high percentage of the cases.[22][23] As such, the researchers stated, "although oxandrolone cannot be implicated as stimulatory [in] gynecomastia", a possible relationship should be considered in clinicians using oxandrolone in adolescents for growth stimulation.[22][23]

Uniquely among 17-alkylated AAS, oxandrolone shows little to no hepatotoxicity, even at high doses.[7][unreliable medical source?][24] No cases of severe hepatotoxicity have been singularly attributed to oxandrolone.[24] However, elevated liver enzymes have been observed in some people, particularly with high doses and/or prolonged treatment, although they return to normal ranges following discontinuation.[24] In any case, oxandrolone may be among the safest 17-alkylated AASs in terms of hepatotoxicity.[7][unreliable medical source?]

Oxandrolone greatly increases warfarin's blood-thinning effect, sometimes dangerously so.[25] In April 2004, Savient Pharmaceuticals published a safety alert through the FDA warning healthcare professionals of this.[26] Oxandrolone can also inhibit the metabolism of oral hypoglycemic agents.[14] It may worsen edema when taken alongside corticosteroids or adrenocorticotropic hormone.[14]

Like other AASs, oxandrolone is an agonist of the androgen receptor, similar to androgens such as testosterone and DHT.[4] This increases protein synthesis, which increases muscle growth, lean body mass, and bone mineral density.[6]

Compared to testosterone and many other AASs, oxandrolone is less androgenic relative to its strength as an anabolic.[4][27] Oxandrolone has about 322 to 633% of the anabolic potency and 24% of the androgenic potency of methyltestosterone.[4] Similarly, oxandrolone has as much as 6times the anabolic potency of testosterone and has significantly reduced androgenic potency in comparison.[4] The reduced ratio of anabolic to androgenic activity of oxandrolone often motivates its medical use in children and women because less androgenic effect implies less risk of virilization.[4] The bodybuilding community also considers this fact when choosing between AASs.[4]

As oxandrolone is already 5-reduced, it is not a substrate for 5-reductase, hence is not potentiated in androgenic tissues such as the skin, hair follicles, and prostate gland.[4] This is involved in its reduced ratio of anabolic to androgenic activity.[4] Due to the substitution of one of the carbon atoms with an oxygen atom at the C2 position in the A ring, oxandrolone is resistant to inactivation by 3-hydroxysteroid dehydrogenase in skeletal muscle.[4] This is in contrast to DHT, and is thought to underlie the preserved anabolic potency with oxandrolone.[4] Because it is 5-reduced, oxandrolone is not a substrate for aromatase, hence cannot be aromatized into metabolites with estrogenic activity.[4] Oxandrolone similarly possesses no progestogenic activity.[4]

Oxandrolone is, uniquely, far less hepatotoxic than other 17-alkylated AASs, which may be due to differences in metabolism.[24][4][1][3]

The oral bioavailability of oxandrolone is 97%.[2] Its plasma protein binding is 94 to 97%.[2] The drug is metabolized primarily by the kidneys and to a lesser extent by the liver.[1][2] Oxandrolone is the only AAS that is not primarily or extensively metabolized by the liver, and this is thought to be related to its diminished hepatotoxicity relative to other AAS.[1][3] Its elimination half-life is reported as 9.4 to 10.4hours, but is extended to 13.3hours in the elderly.[2][3] About 28% of an oral dose of oxandrolone is eliminated unchanged in the urine and 3% is excreted in the feces.[3]

Oxandrolone is a synthetic androstane steroid and a 17-alkylated derivative of DHT.[28][29][4] It is also known as 2-oxa-17-methyl-5-dihydrotestosterone (2-oxa-17-methyl-DHT) or as 2-oxa-17-methyl-5-androstan-17-ol-3-one, and is DHT with a methyl group at the C17 position and the C2 carbon replaced with an oxygen atom.[28][29][4] Closely related AASs include the marketed AAS mestanolone (17-methyl-DHT), oxymetholone (2-hydroxymethylene-17-methyl-DHT), and stanozolol (a 2,3-pyrazole A ring-fused derivative of 17-methyl-DHT) and the never-marketed/designer AAS desoxymethyltestosterone (3-deketo-17-methyl-2-DHT), methasterone (2,17-dimethyl-DHT), methyl-1-testosterone (17-methyl-1-DHT), and methylstenbolone (2,17-dimethyl-1-DHT).[28][29][4]

Oxandrolone was first made by Raphael Pappo and Christopher J. Jung while at Searle Laboratories (now part of Pfizer). The researchers first described the drug in 1962.[4][30][31] They were immediately interested in oxandrolone's very weak androgenic effects relative to its anabolic effects.[30][4] It was introduced as a pharmaceutical drug in the United States in 1964.[4]

The drug was prescribed to promote muscle regrowth in disorders which cause involuntary weight loss, and is used as part of treatment for HIV/AIDS.[4] It had also been shown to be partially successful in treating cases of osteoporosis.[4] However, in part due to bad publicity from its illicit use by bodybuilders, production of Anavar was discontinued by Searle Laboratories in 1989.[4] It was picked up by Bio-Technology General Corporation, which changed its name to Savient Pharmaceuticals, which following successful clinical trials in 1995, released it under the brand name Oxandrin.[4] BTG subsequently won approvals for orphan drug status by the Food and Drug Administration for treating alcoholic hepatitis, Turner syndrome, and HIV-induced weight loss.[4] It is also indicated as an offset to protein catabolism caused by long-term administration of corticosteroids.[4]

Oxandrolone is the generic name of the drug and its INN, USAN, USP, BAN, DCF, DCIT, and JAN, while ossandrolone is or was formerly the DCIT.[28][29][32][9][33]

The original brand name of oxandrolone was Anavar, which was marketed in the United States and the Netherlands.[4][34] This product was eventually discontinued and replaced in the United States with a new product named Oxandrin, which is the sole remaining brand name for oxandrolone in the United States.[4][35] Oxandrolone has also been sold under the brand names Antitriol (Spain), Anatrophill (France), Lipidex (Brazil), Lonavar (Argentina, Australia, Italy), Protivar, and Vasorome (Japan), among others.[4][29][34][36] Additional brand names exist for products that are manufactured for the steroid black market.[4]

Among those using oxandrolone for nonmedical purposes, it is often referred to colloquially as "Var", a shortened form of the brand name Anavar.[37][38][39][self-published source]

Oxandrolone is one of the few AASs that remain available for medical use in the United States.[35] The others (as of November 2017) are testosterone, testosterone cypionate, testosterone enanthate, testosterone undecanoate, methyltestosterone, fluoxymesterone, nandrolone decanoate, and oxymetholone.[35]

Outside of the United States, the availability of oxandrolone is quite limited.[4][9] With the exception of Moldova, it is no longer available in Europe.[4] Oxandrolone is available in some less-regulated markets in Asia such as Malaysia.[4] It is also available in Mexico.[4] Historically, oxandrolone has been marketed in Argentina, Australia, Brazil, France, Italy, Japan, and Spain, but it appears to no longer be available in these countries.[4][29][34][9]

In the United States, oxandrolone is categorized as a Schedule III controlled substance under the Controlled Substances Act along with many other AASs.[11] It is a Schedule IV controlled substance in Canada,[12] and a Schedule 4 controlled drug in the United Kingdom.[13]

Oxandrolone is sometimes used as a doping agent in sports. Cases of doping with oxandrolone by professional athletes have been reported.

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Dec 8th, 2018 | Filed under Testosterone

Most men who require hormone replacement therapy with testosterone have some form of testicular injury or primary hypogonadism. In other words, the problem is all in their balls. Those of us who have secondary hypogonadism often have perfectly functioning testes, but the problem lies elsewhere in whats known as the Hypothalamus Pituitary Testicular Axis (HPTA), which is responsible for keeping our male hormones in proper balance.

The problem with secondary hypogonadism, is that the treatment actually CAUSES primary hypogonadism by introducing exogenous (external) testosterone into the system. To understand that, first lets go over some basics

Hypothalamus:Among other things, this part of your brain sends GnRH (gonadotropin releasing hormone) down to instruct the pituitary gland to create more LH and FSH.

Pituitary Gland:Among other things (like growth hormone), this gland at the base of your brain secretes LH (luteinizing hormone) and FSH (follicle stimulating hormone), which travel down to the testes / gonads to instruct them to create more testosterone.

Testes / Gonads:Endocrinologists might get upset that I use these terms interchangeably. Oh well, screw em. You get the point. Your balls get the message from your pituitary gland to make more testosterone.

The Axis:The important thing to remember about the hypothalamus pituitary testicular axis (HPTA), also sometimes called thehypothalamic-pituitary-gonadal axis (HPG), is that it does not run only in one direction. The body tries to reach homeostasis a healthy balance of these hormones and the entire system can fall out of whack once you start introducing any of these hormones from outside sources. Which brings me to

The Problem With Taking Testosterone to Treat Secondary Hypogonadism:First of all, lets be clear I take testosterone to treat my secondary hypogonadism. Thats because there is currently no choice. Why cure something when you can have a customer for life? Why treat my bodys inability to create enough GnRH when that would require research money and you already have a product that fixes my symptoms ?

Digression aside, the problem with introducing an external source of testosterone is that eventually your gonads see that they are no longer needed. They pack their bags, or rather pack INTO their bags, and practically disappear over time. Now guess what? Not only do I have secondary hypogonadism, which might have been made even worse, but I now have a classic case of primary hypogonadism to deal with if I the medical community should ever find a treatment for secondary hypogonadism.

Heres an idea Why dont pharmaceutical companies make GnRH and market that to the endocrinologists so they can treat the source of my problem? Am I being naive here? Is there more to it than my not-medically-trained mind understands?

All gripes aside, I do feel great. Sure Ill be tied to this drug like a prisoner for the rest of my life, but I feel ten years younger. Im happy, confident, strong, lean, sharp, motivated, and a lot more fun in the bedroom. And Ive yet to see any CONVINCING studies about the long-term health dangers of testosterone replacement in hypogonadal men. Heart disease? Prostate cancer? Show me the studies? These are often-quoted side-effects, but all I hear are doctors deducing them because, for instance, taking away a mans testosterone seems to help with pre-existing conditions of prostate cancer. But that is not a cause-and-effect relationship. Just because removing testosterone helps treat or minimizes the recurrence of prostate cancer, doesnt mean it causes prostate cancer. Does it? OK, ok, thats anothe post entirely

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Dec 7th, 2018 | Filed under Testosterone

abortion

A procedure to intentionally end a pregnancy before a birth. Miscarriage is also sometimes called "spontaneous abortion," even though it is usually not intended.

Purposeful harm or mistreatment of another person, which can be verbal, emotional, physical or sexual. An ongoing pattern or cycle of such mistreatment or harm can characterize an abusive relationship.

In the context of sexuality, an abbreviation for asexual.

People older than you who probably drive you batty. Or, people whose age in years exceeds the legal age of majority; people considered to be adults by law.

A state or demonstration of fondness or care for someone, which may or may not be sexual.

The age at which a person is considered in law to be able to consent to sexual activity. Someone above this age who has sex with someone below it can often be charged with statutory rape, even if the younger person wants to consent.

When two people are of different ages or life stages, usually with a substantial difference.

A chosen or felt lack of gender identity.

Behaving in a pushy, forceful or violent way.

Acquired immune deficiency syndrome (AIDS) is a very serious and often deadly disease of the immune system caused by HIV. AIDS itself can not be caught from another person, but those with AIDS have HIV, which is sexually transmissible. AIDS requires medical treatment.

When a penis is inserted into and held by the anus while partners move their bodies as feels good to them for the purpose of sexual stimulation.

Sexual activity involving the anus. Anal sex may include stimulation with fingers, the mouth, a penis, sex toys, or other objects or body parts.

Oral sex for, on or to the anus.

The body, parts of the body, or physical structure of organisms like people, animals or plants.

Being neither distinguishably masculine nor feminine (or a mishmosh of both), in dress, appearance, behavior or identity, either by choice or by circumstance.

The external opening to the rectum, located between the buttocks.

Not having an interest in romantic relationships.

A state of sexual excitement and interest that sends messages to the brain which create physical changes and sensations, such as increased blood pressure, erection, lubrication, loosening of the vaginal or anal muscles, and increased physical sensitivity.

In the context of human sexuality, someone who either does not experience or has not yet experienced any sexual desires at all, or who has experienced/does experience sexual desires, but not a desire to enact them with other individuals.

To be self-assured, self-confident. To stand up for oneself in a positive, nonviolent way.

The state or condition of being independent and/or having the right to independence.

An imbalance in the vaginal environment, including pH changes, that occurs when different types of bacteria outnumber the normal, needed and healthy bacteria. It often requires some from of treatment, but sometimes will go away on its own.

Describes sexual play and/or relationships involving exchanges of power and pain. B = bondage, D = discipline and/or dominance, S = submission and/or sadism, M = masochism.

Made up of two things or parts; a system with only two possible options or parts.

Prejudice against bisexuality and bisexual people.

Any number of methods people use to intentionally prevent unwanted pregnancy, including the condom, the cervical barrier, the implant, the patch, the pill, the rhythm method, the ring, the shot, the IUD, spermicide and withdrawal.

A term for sexual orientation which either describes a person who can be sexually and emotionally attracted to both men and women or merely to people of more than one gender.

A stage of very early fetal development. If cell development continues and a blastocyst implants in the uterus, it will become an embryo and create a pregnancy.

A slang term for a state of vasocongestion that becomes temporarily painful. Called "blue balls" because in those with testes, discomfort is also felt there, but people with vulvas can experience this too, and discomfort then is often felt in the uterus or clitoris.

Our sense, awareness and perception of our body in appearance and function as it relates to our sense of self.

Glandular tissue, fat, connective tissue and skin on the chest.

Describes a person who is intentionally masculine in appearance, behavior, dress, identity or sexual attitude. Often used in relation to femme. Most often used in the LGBT community, but can refer to people of any orientation. However, some people see use of the word "butch" as an insult.

Describes someone who does not engage in sexual activity, usually by choice.

A birth control device which is inserted into the vagina to cover the cervix and prevent sperm from entering. Diaphragms, cervical caps and contraceptive sponges are kinds of cervical barriers.

The opening to the uterus, the bottom of which is at the back end of the vagina.

A method of keeping track of fertility by keeping careful notes on the dates of a woman's period, as well as her temperature and cervical mucus. This is often used by people who are trying to get pregnant but is NOT an effective birth control method, as it fails frequently due to fluctuations in a woman's cycle and the fact that sperm can live in a woman's reproductive tract for several days. Also called "fertility awareness".

A slang term used to describe either the hymen/corona or something which signifies someone has not done something for the first time. "Popping the cherry" often describes doing something sexual for the first time, even though with first-time sex, there are not usually cherries or the popping of anything.

A very common bacterial infection/STI. It can infect the cervix, urethra, testicles, fallopian tubes, and/or ovaries. It can also infect the throat when acquired through oral sex. Chlamydia requires medical treatment.

A surgical removal of the foreskin from the penis, most often done in infancy, and most often done because of cultural or religious beliefs, parental aesthetic preferences or concerns about health. In some cases, circumcision is done at other times of life and/or for medical reasons.

Describes people who have a gender identity which is traditionally thought to match their assigned sex, and thought to match many or most of the roles, behaviors and appearances culturally expected of that sex. For example, someone who was sexed male at birth and whose gender identity is masculine; who also feels male. Often used in relation to transgender.

Prejudice, discrimination and oppression based on social or economic status/class or perceived or assigned social or economic status.

In a sexual context, usually a word used to suggest not having any sexually transmitted infections. "Clean" is a poor choice of term, however, since it stigmatizes people with illness. Better choices are "negative," "clear" or "STI-free."

A sexual organ both external and internal on the vulva and inside the pelvis of female sex-assigned people that is similar to the penis, but serves no other known purpose besides providing sexual pleasure.

Various ways we express and share feelings or thoughts, such as through speech, written words or symbols, sign language, body language, touch or art.

The onset of pregnancy, marked by implantation of the blastocyst into the endometrium (the lining of the uterus).

A thin sheath or tube of latex or another material, worn over the penis during sex to prevent or reduce the risk of pregnancy and/or sexually transmitted infections.

To agree to do something or give permission. In the context of sex, a person is giving full consent/is consenting when they freely and actively agree to do something sexual with someone else; however, the person still has the right to change their mind at any point. A person is NOT consenting if they do not actively agree, have been forced or pressured in some way or are in a state where they are incapable of full consent (such as when asleep, under the influence of drugs or alcohol, or below the age of consent).

Devices, medications or behaviors used to intentionally aim to prevent pregnancy, including the condom, the cervical barrier, the implant, the patch, the pill, the rhythm method, the ring, the shot, the IUD, spermicide and withdrawal.

A method of birth control that consists of a spongy device filled with spermicide that provides a barrier at the entrance of the cervix.

A newer name for the hymen, a thin membrane without nerve endings that most female-assigned people are born with that is just inside the vaginal opening. It gradually wears away over time due to hormones, vaginal discharges, general physical activity, sex and masturbation and/or childbirth. It does not snap, crackle or pop.

The internal "legs" of the clitoris, which are within the outer labia (labia majora).

Oral sex for, on or to the vulva.

Heather's pug, Sofia.

Virtual (as in, not in person) sexual experiences or encounters which involve text conversations and/or visual exchanges via the Internet.

CMV is one member of a group of herpes-type viruses. It is an STI transmitted through body fluids, and requires medical treatment.

How well something works.

In a sexual context, a discharge of genital fluid, usually (but not always) as a result of sexual stimulation and/or orgasm.

During a pregnancy, the term for the developing cells of an organism until around eight-nine weeks after an ovum was fertilized. After this time, the organism would then be called a fetus.

A method of contraception used to prevent pregnancy after sex or rape has already occurred, rather than used before or during, like most types of contraception.

To put something into action: to actively do something, not just think or feel it.

The lining of the uterus.

In a sexual context, when a kind of sex involves someone putting one body part inside the body part of another person, such as with intercourse. Some people use the word "penetration" instead.

When a body part, such as the penis or parts of the vulva, becomes filled with blood and enlarges and/or becomes more firm.

Various areas of the body with a greater number of sensory nerve receptors than other areas, which people may find particularly sexually stimulating, such as (but by no means limited to) the lips, tongue, palms, fingers, feet, inner thighs, anus, nipples, neck, collarbone, nose, ears, armpits and/or the genitals.

Written, visual or other kinds of media either expressly designed to elicit feelings of sexual desire and/or which people use to elicit those feelings.

A steroid hormone found in the bodies of all people which has several jobs. Like testosterone, people often say it's responsible for things it doesn't usually have much to do with (like mood).

Something that is not divided or shared with others; which excludes others based on a given criteria.

Two tubes that lead from the ovaries to the uterus. If and when an ovum is fertilized by a sperm, fertilization typically happens within the fallopian tube.

Fertility awareness methods of birth control, achieved by charting of fertility, ideally daily via cervical mucus and basal body temperatures, and interpreting that charting to determine when fertility is most and least likely, then abstaining or using a backup method during most fertile times.

Oral sex for, on or to the penis.

A barrier method of contraception somewhat similar to a male condom, but inserted into the vagina rather than put on the penis. It has a flared base that sits on the outer parts of the vulva to hold it in place.

Describes something society associates with or attributes to women and girls or a state, experience or assignment of being female.

Describes a person who is intentionally feminine in appearance, behavior, dress, identity or sexual attitude. Often used in relation to butch. Most often used in the LGBT community, but can refer to people of any orientation.

A method of keeping track of fertility by keeping careful notes on the dates of a woman's period, as well as her temperature and cervical mucus. This is often used by people who are trying to get pregnant but is NOT an effective birth control method, as it fails frequently due to fluctuations in a woman's cycle and the fact that sperm can live in a woman's reproductive tract for several days. Also called "fertility charting" or just "charting".

In humans, the stage of prenatal development after an embryo, usually from about the eighth-ninth week after fertilization.

A term used to describe deep manual sex, where many fingers or a hand are gradually inserted into the vagina or anus.

What some people call sexual activities that are not intercourse which they may do before intercourse or as a "warmup" to intercourse, such as kissing, manual sex or oral sex. However, all kinds of "foreplay" can also be or are kinds of sex, and may sometimes be the only sex people choose to or can engage in at a given time, or altogether.

A loose tube of skin with nerve endings that extends from shaft of the penis to below the glans and which normally covers the head of the penis when it is not erect. Those born with penises are also born with a foreskin, but some foreskins are removed (circumcised) in infancy or later in life for any of a variety of different reasons.

A small fold of skin at the posterior (bottom) end of the vulva.

People who have a sexual relationship that is not romantic, but where they are also (and are supposed to behave like) friends. Often a casual relationship, but not always. FWBs may or may not be exclusive.

Rubbing against the body of another person -- usually with clothes on -- to express sexual feelings or seek out sexual pleasure. "Dry humping" is a form of frottage.

Friends with benefits.

A portion of the internal clitoris 1-3 inches within the vagina on the anterior (front) wall which can be sexually stimulating and which is often associated with female ejaculation.

In the context of sexuality, a word for sexual orientation which either describes a man who is sexually and emotionally attracted to other men, or a person of any sex or gender who is sexually and emotionally attracted to people of the same or a similar sex or gender. Often used alongside lesbian.

Characteristics that are seen or presented as distinguishing between male and female. Gender may or may not include assigned or chosen: sex, social roles, feelings, behaviors and/or presentation or appearance.

Discomfort with an assigned sex and/or gender and/or the gender norms and roles associated with either.

The way people externally communicate gender identity to others through their behavior and their outward, chosen appearance.

A person's own sense of whether and in what sense they feel they might be a man, a woman, a boy, a girl or gender nonconforming.

People who do not adhere to or who protest cultural rules or norms about dress, behaviors or activities for people based on their sex.

What is considered "normal" for a given gender or sex, even if it's not. These ideas may be widespread, or may be specific to a given group, area or historical period of time.

Describes someone whose chosen gender identity is neither masculine nor feminine, is between or beyond genders, which rejects binary gender, or which is some combination of genders.

Kinds of sex people have which involve the vulva, vagina, penis, testicles, anus and/or rectum or any immediate areas surrounding those parts.

External sexual or reproductive organs.

On the penis, the head of the penis. On the vulva, the external portion of the clitoris, beneath the clitoral hood.

G = gay, L = lesbian, B = bisexual, T = transgender. Additional letters sometimes added include Q = queer/questioning, U = unsure, I = intersex, P = pansexual, S = straight allies.

The organs that make ovum or sperm cells (the ovaries and testes respectively).

A bacterial infection/STI which can infect the cervix, uterus, fallopian tubes, urethra, mouth, throat or anus. It requires medical treatment.

An exam usually for those with a vulva/vagina that may involve any of the following: a visual exam of the genitals, a breast exam, a bimanual exam, a speculum exam, a pap smear, STI testing, birth control consultation and other education or healthcare services.

(Pronounced guy-na-coll-o-jist) A doctor that specializes in the health of the female reproductive tract. They may also be referred to as "OB/GYNs" or, informally, "gynos".

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Glossary | Scarleteen

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Dec 7th, 2018 | Filed under Testosterone

What is a testosterone levels test?

Testosterone is the main sex hormone in males. During a boy's puberty, testosterone causes the growth of body hair, muscle development, and deepening of the voice. In adult men, it controls sex drive, maintains muscle mass, and helps make sperm. Women also have testosterone in their bodies, but in much smaller amounts.

This test measures the levels of testosterone in your blood. Most of the testosterone in the blood is attached to proteins. Testosterone that is not attached to a protein is called free testosterone. There are two main types of testosterone tests:

Testosterone levels that are too low (low T) or too high (high T) can cause health problems in both men and women.

Other names: serum testosterone, total testosterone, free testosterone, bioavailable testosterone

A testosterone levels test may be used to diagnose several conditions, including:

You may need this test if you have symptoms of abnormal testosterone levels. For adult men, it's mostly ordered if there are symptoms of low T levels. For women, it's mostly ordered if there are symptoms of high T levels.

Symptoms of low T levels in men include:

Symptoms of high T levels in women include:

Boys may also need a testosterone levels test. In boys, delayed puberty can be a symptom of low T , while early puberty may be a symptom of high T.

A health care professional will take a blood sample from a vein in your arm, using a small needle. After the needle is inserted, a small amount of blood will be collected into a test tube or vial. You may feel a little sting when the needle goes in or out. This usually takes less than five minutes.

You don't need any special preparations for a testosterone levels test.

There is very little risk to having a blood test. You may have slight pain or bruising at the spot where the needle was put in, but most symptoms go away quickly.

Results mean different things depending on whether you are a man, woman, or boy.

For men:

For women:

For boys:

If your results are not normal, it doesn't necessarily mean you have a medical condition needing treatment. Certain medicines, as well as alcoholism, can affect your results. If you have questions about your results, talk to your health care provider.

Men who are diagnosed with low T levels may benefit from testosterone supplements, as prescribed by their health care provider. Testosterone supplements are not recommended for men with normal T levels. There is no proof they provide any benefits, and in fact they may be harmful to healthy men.

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Testosterone Levels Test: MedlinePlus Lab Test Information

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Dec 5th, 2018 | Filed under Testosterone

This article is about dihydrotestosterone as a hormone. For its use as a medication, see Androstanolone.This article is about 5-dihydrotestosterone, an androgen. For the inactive 5 isomer, see 5-Dihydrotestosterone.DihydrotestosteroneNamesIUPAC name

(5S,8R,9S,10S,13S,14S,17S)-17-Hydroxy-10,13-dimethyl-1,2,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydrocyclopenta[a]phenanthren-3-one

DHT; 5-Dihydrotestosterone; 5-DHT; Androstanolone; Stanolone; 5-Androstan-17-ol-3-one

O=C4C[C@@H]3CC[C@@H]2[C@H](CC[C@]1(C)[C@@H](O)CC[C@H]12)[C@@]3(C)CC4

Dihydrotestosterone (DHT, 5-dihydrotestosterone, 5-DHT, androstanolone or stanolone) is an endogenous androgen sex steroid and hormone. The enzyme 5-reductase catalyzes the formation of DHT from testosterone in certain tissues including the prostate gland, seminal vesicles, epididymides, skin, hair follicles, liver, and brain. This enzyme mediates reduction of the C4-5 double bond of testosterone. Relative to testosterone, DHT is considerably more potent as an agonist of the androgen receptor (AR).

In addition to its role as a natural hormone, DHT has been used as a medication, for instance in the treatment of low testosterone levels in men; for information on DHT as a medication, see the androstanolone article.

DHT is biologically important for sexual differentiation of the male genitalia during embryogenesis, maturation of the penis and scrotum at puberty, growth of facial, body, and pubic hair, and development and maintenance of the prostate gland and seminal vesicles. It is produced from the less potent testosterone by the enzyme 5-reductase in select tissues, and is the primary androgen in the genitals, prostate gland, seminal vesicles, skin, and hair follicles.[2]

DHT signals mainly in an intracrine and paracrine manner in the tissues in which it is produced, playing only a minor role, if any, as a circulating endocrine hormone.[3][4][5] Circulating levels of DHT are 1/10th and 1/20th those of testosterone in terms of total and free concentrations, respectively,[6] whereas local DHT levels may be up to 10times those of testosterone in tissues with high 5-reductase expression such as the prostate gland.[7] In addition, unlike testosterone, DHT is inactivated by 3-hydroxysteroid dehydrogenase (3-HSD) into the very weak androgen 3-androstanediol in various tissues such as muscle, adipose, and liver among others,[5][8][9] and in relation to this, DHT has been reported to be a very poor anabolic agent when administered exogenously as a medication.[10]

In addition to normal biological functions, DHT also plays an important causative role in a number of androgen-dependent conditions including hair conditions like hirsutism (excessive facial/body hair growth) and pattern hair loss (androgenic alopecia or pattern baldness) and prostate diseases such as benign prostatic hyperplasia (BPH) and prostate cancer.[2] 5-Reductase inhibitors, which prevent DHT synthesis, are effective in the prevention and treatment of these conditions.[13][14][15][16]

Metabolites of DHT have been found to act as neurosteroids with their own AR-independent biological activity.[17] 3-Androstanediol is a potent positive allosteric modulator of the GABAA receptor, while 3-androstanediol is a potent and selective agonist of the estrogen receptor (ER) subtype ER.[17] These metabolites may play important roles in the central effects of DHT and by extension testosterone, including their antidepressant, anxiolytic, rewarding/hedonic, anti-stress, and pro-cognitive effects.[17][18]

Much of the biological role of DHT has been elucidated in studies of individuals with congenital 5-reductase type II deficiency, an intersex condition caused by a loss-of-function mutation in the gene encoding 5-reductase type II, the major enzyme responsible for the production of DHT in the body.[13][19][2] It is characterized by a defective and non-functional 5-reductase type II enzyme and a partial but majority loss of DHT production in the body.[13][19] In the condition, circulating testosterone levels are within or slightly above the normal male range, but DHT levels are low (around 30% of normal),[20][bettersourceneeded] and the ratio of circulating testosterone to DHT is greatly elevated (at about 3.5 to 5times higher than normal).[13]

Genetic males (46,XY) with 5-reductase type II deficiency are born with undervirilization including pseudohermaphroditism (ambiguous genitalia), pseudovaginal perineoscrotal hypospadias, and usually undescended testes. Their external genitalia are female-like, with micropenis (a small, clitoris-like phallus), a partially unfused, labia-like scrotum, and a blind-ending, shallow vaginal pouch.[13] Due to their lack of conspicuous male genitalia, genetic males with the condition are typically raised as girls.[19] At the time of puberty however, they develop striking phenotypically masculine secondary sexual characteristics including partial virilization of the genitals (enlargement of the phallus into a near-functional penis and descent of the testes), voice deepening, typical male musculoskeletal development,[12] and no menstruation, breast development, or other signs of feminization that occur during female puberty.[13][19][2] In addition, normal libido and spontaneous erections develop,[21] they usually show a sexual preference for females, and almost all develop a male gender identity.[13][22]

Nonetheless, males with 5-reductase type II deficiency exhibit signs of continued undervirilization in a number of domains. Facial hair was absent or sparse in a relatively large group of Dominican males with the condition. However, more facial hair has been observed in patients with the disorder from other parts of the world, although facial hair was still reduced relative to that of other men in the same communities. The divergent findings may reflect racial differences in androgen-dependent hair growth. A female pattern of androgenic hair growth, with terminal hair largely restricted to the axillae and lower pubic triangle, is observed in males with the condition. No temporal recession of the hairline or androgenic alopecia (pattern hair loss or baldness) has been observed in any of the cases of 5-reductase type II deficiency that have been reported, whereas this is normally seen to some degree in almost all Caucasian males.[13] Individuals with 5-reductase type II deficiency were initially reported to have no incidence of acne,[8][2] but subsequent research indicated normal sebum secretion and acne incidence.[12]

In genetic males with 5-reductase type II deficiency, the prostate gland is rudimentary or absent, and if present, remains small, underdeveloped, and unpalpable throughout life.[8][4] In addition, neither BPH nor prostate cancer have been reported in these individuals.[14] Genetic males with the condition generally show oligozoospermia due to undescended testes, but spermatogenesis is reported to be normal in those with testes that have descended, and there are case instances of men with the condition successfully fathering children.[21][23]

Unlike males, genetic females with 5-reductase type II deficiency are phenotypically normal. However, similarly to genetic males with the condition, they show reduced body hair growth, including an absence of hair on the arms and legs, slightly decreased axillary hair, and moderately decreased pubic hair.[24][21] On the other hand, sebum production is normal.[24][25] This is in accordance with the fact that sebum secretion appears to be entirely under the control of 5-reductase type I.[25]

5-Reductase inhibitors like finasteride and dutasteride inhibit 5-reductase type II and/or other isoforms and are able to decrease circulating DHT levels by 65 to 98% depending on the 5-reductase inhibitor in question.[26][27][28][20] As such, similarly to the case of 5-reductase type II deficiency, they provide useful insights in the elucidation of the biological functions of DHT.[29] 5-Reductase inhibitors were developed and are used primarily for the treatment of BPH. The drugs are able to significantly reduce the size of the prostate gland and to alleviate symptoms of the condition.[14][30] Long-term treatment with 5-reductase inhibitors is also able to significantly reduce the overall risk of prostate cancer, although a simultaneous small increase in the risk of certain high-grade tumors has been observed.[15] In addition to prostate diseases, 5-reductase inhibitors have subsequently been developed and introduced for the treatment of pattern hair loss in men.[31] They are able to prevent further progression of hair loss in most men with the condition and to produce some recovery of hair in about two-thirds of men.[13] 5-Reductase inhibitors seem to be less effective for pattern hair loss in women on the other hand, although they do still show some effectiveness.[32] Aside from pattern hair loss, the drugs are also useful in the treatment of hirsutism and can greatly reduce facial and body hair growth in women with the condition.[33][16]

5-Reductase inhibitors are overall well-tolerated and show a low incidence of adverse effects.[34] Sexual dysfunction, including erectile dysfunction, loss of libido, and reduced ejaculate volume, may occur in 3.4 to 15.8% of men treated with finasteride or dutasteride.[34][35] A small increase in the risk of affective symptoms including depression, anxiety, and self-harm may be seen.[36][37][38] Both the sexual dysfunction and affective symptoms may be due partially or fully to prevention of the synthesis of neurosteroids like allopregnanolone rather necessarily than due to inhibition of DHT production.[36] A very small risk of gynecomastia has been associated with 5-reductase inhibitors (1.2 to 3.5%).[34][39] Based on reports of 5-reductase type II deficiency in males and the effectiveness of 5-reductase inhibitors for hirsutism in women, reduced body and/or facial hair growth is a likely potential side effect of these drugs in men.[13][16] There are very few studies evaluating the side effects of 5-reductase inhibitors in women. However, due to the known role of DHT in male sexual differentiation, 5-reductase inhibitors may cause birth defects such as ambiguous genitalia in the male fetuses of pregnant women. As such, they are not used in women during pregnancy.[34]

MK-386 is a selective 5-reductase type I inhibitor which was never marketed.[40] Whereas 5-reductase type II inhibitors achieve much higher reductions in circulating DHT production, MK-386 decreases circulating DHT levels by 20 to 30%.[41] Conversely, it was found to decrease sebum DHT levels by 55% in men versus a modest reduction of only 15% for finasteride.[42][43] However, MK-386 failed to show significant effectiveness in a subsequent clinical study for the treatment of acne.[44]

DHT is a potent agonist of the AR, and is in fact the most potent known endogenous ligand of the receptor. It has an affinity (Kd) of 0.25 to 0.5nM for the human AR, which is about 2- to 3-fold higher than that of testosterone (Kd = 0.4 to 1.0nM)[45] and 1530times higher than that of adrenal androgens.[46] In addition, the dissociation rate of DHT from the AR is 5-fold slower than that of testosterone.[47] The EC50 of DHT for activation of the AR is 0.13nM, which is about 5-fold stronger than that of testosterone (EC50 = 0.66nM).[48] In bioassays, DHT has been found to be 2.5- to 10-fold more potent than testosterone.[45]

The terminal half-life of DHT in the body (53minutes) is longer than that of testosterone (34minutes), and this may account for some of the difference in their potency.[49] A study of transdermal DHT and testosterone treatment reported terminal half-lives of 2.83hours and 1.29hours, respectively.[50]

Unlike other androgens such as testosterone, DHT cannot be converted by the enzyme aromatase into an estrogen like estradiol. Therefore, it is frequently used in research settings to distinguish between the effects of testosterone caused by binding to the AR and those caused by testosterone's conversion to estradiol and subsequent binding to and activation of ERs.[51] Although DHT cannot be aromatized, it is still transformed into metabolites with significant ER affinity and activity. These are 3-androstanediol and 3-androstanediol, which are predominant agonists of the ER.[17]

DHT is synthesized irreversibly from testosterone by the enzyme 5-reductase.[8][13] This occurs in various tissues including the genitals (penis, scrotum, clitoris, labia majora),[53] prostate gland, skin, hair follicles, liver, and brain.[8] Around 5 to 7% of testosterone undergoes 5-reduction into DHT,[54][55] and approximately 200 to 300g of DHT is synthesized in the body per day. Most DHT is produced in peripheral tissues like the skin and liver, whereas most circulating DHT originates specifically from the liver. The testes and prostate gland contribute relatively little to concentrations of DHT in circulation.[8]

There are two major isoforms of 5-reductase, SRD5A1 (type I) and SRD5A2 (type II), with the latter being the most biologically important isoenzyme.[8] There is also third 5-reductase: SRD5A3.[56] SRD5A2 is most highly expressed in the genitals, prostate gland, epididymides, seminal vesicles, genital skin, facial and chest hair follicles,[57][58] and liver, while lower expression is observed in certain brain areas, non-genital skin/hair follicles, testes, and kidneys. SRD5A1 is most highly expressed in non-genital skin/hair follicles, the liver, and certain brain areas, while lower levels are present in the prostate, epididymides, seminal vesicles, genital skin, testes, adrenal glands, and kidneys.[8] In the skin, 5-reductase is expressed in sebaceous glands, sweat glands, epidermal cells, and hair follicles.[57][58] Both isoenzymes are expressed in scalp hair follicles,[59] although SRD5A2 predominates in these cells.[58] The SRD5A2 subtype is the almost exclusive isoform expressed in the prostate gland.[60][20]

The plasma protein binding of DHT is more than 99%. In men, approximately 0.88% of DHT is unbound and hence free, while in premenopausal women, about 0.470.48% is unbound. In men, DHT is bound 49.7% to sex hormone-binding globulin (SHBG), 39.2% to albumin, and 0.22% to corticosteroid-binding globulin (CBG), while in premenopausal women, DHT is bound 78.178.4% to SHBG, 21.021.3% to albumin, and 0.12% to CBG. In late pregnancy, only 0.07% of DHT is unbound in women; 97.8% is bound to SHBG while 2.15% is bound to albumin and 0.04% is bound to CBG.[61][62] DHT has higher affinity for SHBG than does testosterone, estradiol, or any other steroid hormone.[63][62]

DHT is inactivated in the liver and extrahepatic tissues like the skin into 3-androstanediol and 3-androstanediol by the enzymes 3-hydroxysteroid dehydrogenase and 3-hydroxysteroid dehydrogenase, respectively.[8][64] These metabolites are in turn converted, respectively, into androsterone and epiandrosterone, then conjugated (via glucuronidation and/or sulfation), released into circulation, and excreted in urine.[8]

Unlike testosterone, DHT cannot be aromatized into an estrogen like estradiol, and for this reason, has no propensity for estrogenic effects.[65]

DHT is excreted in the urine as metabolites, such as conjugates of 3-androstanediol and androsterone.[66][8]

Serum DHT levels are about 10% of those of testosterone, but levels in the prostate gland are 5- to 10-fold higher than those of testosterone due to a more than 90% conversion of testosterone into DHT by locally expressed 5-reductase.[7] For this reason, and in addition to the fact that DHT is much more potent as an AR agonist than is testosterone,[45] DHT is considered to be the major androgen of the prostate gland.[7]

DHT is available in pharmaceutical formulations for medical use as an androgen or anabolicandrogenic steroid (AAS).[67] It is used mainly in the treatment of male hypogonadism.[68] When used as a medication, dihydrotestosterone is referred to as androstanolone (INN) or as stanolone (BAN),[67][69][70] and is sold under brand names such as Andractim among others.[67][69][70][68][71] The availability of pharmaceutical DHT is limited; it is not available in the United States or Canada,[72][73] but is available in certain European countries.[70][68] The available formulations of DHT include buccal or sublingual tablets, topical gels, and, as esters in oil, injectables like androstanolone propionate and androstanolone valerate.[67][68][71]

DHT, also known as 5-androstan-17-ol-3-one, is a naturally occurring androstane steroid with a ketone group at the C3 position and a hydroxyl group at the C17 position. It is the derivative of testosterone in which the double bond between the C4 and C5 positions has been reduced or hydrogenated.

DHT was first synthesized by Adolf Butenandt and his colleagues in 1935.[74][75] It was prepared via hydrogenation of testosterone,[75] which had been discovered earlier that year.[76] DHT was introduced for medical use as an AAS in 1953, and was noted to be more potent than testosterone but with reduced androgenicity.[77][78][79] It was not elucidated to be an endogenous substance until 1956, when it was shown to be formed from testosterone in rat liver homogenates.[75][80] In addition, the biological importance of DHT was not realized until the early 1960s, when it was found to be produced by 5-reductase from circulating testosterone in target tissues like the prostate gland and seminal vesicles and was found to be more potent than testosterone in bioassays.[81][82][83][84] The biological functions of DHT in humans became much more clearly defined upon the discovery and characterization of 5-reductase type II deficiency in 1974.[14] DHT was the last major sex hormone, the others being testosterone, estradiol, and progesterone, to be discovered, and is unique in that it is the only major sex hormone that functions principally as an intracrine and paracrine hormone rather than as an endocrine hormone.[85]

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Zinc is an essential mineral found in high levels in animal tissues and eggs, legumes, and fish; it is exceptionally high in shellfish such as oyster[2][3] and may also be fortified into cereal grains in developed countries.[4]

Zinc is most commonly touted to be important as it is a cofacter in over 300 enzymes involved in gene expression, cell proliferation and signal transduction[5][6][7] and deficiencies of zinc may reduce the activity of these enzymes.

Zinc's main role in the body is as a prosthetic group for several enzymes called metalloproteins, one of which is the Superoxide Dismustase enzyme; an endogenous anti-oxidant involving both zinc and copper.[8][9][10] Zinc is also involved in regulating the immune system.[11][12]

The RDA values for zinc are an Estimated Average Requirement (EAR) of 6.5mg for females, 8.5-10mg for pregnant or lactating females, and 12mg a day for men. The Recommended Daily Intake (RDI) values are 8mg for females, 10-12mg for pregnant or lactating females, and 14-15mg for males, and the Tolerable Upper intake Limit (TUL) is in the range of 35-40mg for adults of both genders (all numbers daily requirements).[13][14]

A deficiency in zinc is related to delayed growth in youth and hypogonadism in adult males[15] as well as general mental lethargy and skin abnormalities.[16]

When looking at zinc deficiency rates, it has been noted that around 10% of persons (USA) have a dietary intake of less than half the RDA of zinc[17][18] while global deficiency rates are over 50% (due to high deficiency rates in third world countries).[18] It has been reported (WHO, 2002) to be a major factor contributing to 1.4% deaths worldwide associated with severe zinc deficiency in childhood[19] although this magnitude of deficiency is almost never observed in first-world countries.[20]

Zinc is lost during sweat and exercise[21][22] and may be a contributing factor to why testosterone levels seem to be depressed after exhaustive exercise.[23][24]

In diabetic individuals (following information seems to apply equally to type I and type II diabetics), urinary zinc excretion rates are increased[25][26][27] and although serum zinc concentrations are unreliably influenced (increased,[25][28] decreased,[29][30][31] or not different from non-diabetic controls[32]) cellular concentrations of zinc as measured in immune cells (mononuclear cells, granulocytes, lymphocytes and leucocytes) tend to be reduced relative to nondiabetic controls.[29][33][30]

Zinc Citrate, at 50mg elemental Zinc (146mg) daily for 4 weeks is associated with a maintenance of Zinc status while placebo declines over time (told to maintain a low Zinc diet, estimated between 10-12mg).[34]

Zinc Gluconate, at 50mg elemental Zinc (385mg), appears to be slightly more effective than Zinc Citrate (nonsignificant) and can increase serum and erythrocytic stores of Zinc in apparently healthy persons over a period of 4 weeks.[34]

Zinc Picolinate (bound to picolinic acid, a metabolite of tryptophan), at 50mg elemental Zinc (144mg) in healthy persons appears to increase urinary and serum levels greater than placebo and the other two forms tested (Citrate, Gluconate).[34]

Zinc carnosine (ZnC) is a synthetic molecule where zinc and carnosine are linked together in a 1:1 ratio, forming a polymer-structure. The compound has been used for some time in Japan as a treatment for gastritis and gastric ulcers, and studies have shown that ZnC is up to 3 times more effective at promoting gastric integrity than either zinc or carnosine alone.[35] When the integrity of gastrointestinal (GI) tract becomes compromised, intestinal permeability increases which may allow the passage of harmful substances into the blood stream. This can cause an immune response, leading to systemic inflammation. Although not an official medical term, conditions associated with increased intestinal permeability have been termed leaky gut syndrome, which can be caused by food allergies, certain medications and inflammatory bowel disease.[36]

While ZnC is known to protect against increases in intestinal permeability, the mechanisms at work are not entirely clear. One study employed several in vitro and in vivo models to examine the mechanisms behind ZnC protection of the GI tract.[37] To examine the effects of ZnC on wound healing mechanisms that may be important in the context of leaky guy syndrome, HT129 colonic cells were grown to form a cell monolayer covering the entire surface cell culture plates. An artificial wound was then induced by scraping a line through the entire cell monolayer, removing all cells within the scratch. The ability of the cells to migrate back into the scratch, healing the cell monolayer was then tested in the presence or absence of ZnC. ZnC increased cell migration by approximately 100% compared to the vehicle control, suggesting that it may promote gastric healing in part by increasing epithelial cell migration in injured regions of the GI tract.[37] ZnC also induced a dose-dependent increase on cell proliferation, with a maximal response at 100M.[37]

To examine the ability of ZnC to promote gastric healing in vivo, researchers also examined the effects of ZnC in a rat model for gastric damage. Rats were given ZnC (1 or 5 mg/mL) or a placebo prior to 20 mg/kg indomethacin, a non-steroidal anti-inflammatory drug (NSAID) that causes gastric damage. ZnC substantially decreased markers for gastric damage at both 1 and 5 mg/ml, with the 5 mg/ml dose being more effective.[37]

The ability of ZnC to prevent small intestinal damage by indomethacin was also evaluated in mice. In control mice that received indomethacin alone, substantial shortening of intestinal villi were noted, along with decreased intestinal weight, both indicators of damage. In contrast, ZnC treatment reduced indomethacin-induced villus-shortening and increased intestinal weight, indicating a protective effect.

To validate the results obtained with in vitro cell culture studies and animal models, 10 healthy human volunteers were recruited in a double-blind, randomized and placebo controlled study. To assess the effects of ZnC on indomethacin-induced increases in intestinal permeability, participants drank a sugar solution containing a mixture of mono-and disaccharides. Since disaccharides are larger and are not easily absorbed in the GI tract by passive diffusion, an increase in urine disaccharide to monosaccharide ratio indicates increased intestinal permeability due to damage. Subjects took either ZnC (37.5 mg twice daily) or a placebo for seven days, with indomethacin for the last 5 days. When taking a placebo, subjects showed a 3x increase in disaccharide ratio, indicating a substantial increase in intestinal permeability from the indomethacin-induced injury. In contrast, subjects taking ZnC showed no significant increase in disaccharide ratio, indicating a strong protective effect on the gut mucosa.[37]

The regulation of bodily zinc levels tends to occur at the level of the intestines secondary to regulated absorption and fecal excretion[38][39] and in instances of zinc deficiency intestinal absorption can near 100%.[38] This has been replicated in humans where zinc absorption during instances of deficiency and is attenuated with sufficiency.[40][41][42]

At least one animal study has suggested that dysregulation occurs with intestinal zinc absorption during aging, and adequate dietary intake may in turn be metabolically insufficient due to poorer absorption.[43]

Absorption of zinc tends to be regulated, with higher oral intakes being associated with lower bioavailability and approximately 5mg absorbed in postmenopausal women regardless of dietary or supplemental intake.[44]

In otherwise healthy men supplemented with zinc, fasting plasma concentrations can increase within five days of supplementation regardless of baseline zinc status.[45] 10mg and 20mg elemental zinc (syrup) were equivalent in their ability to heighten plasma zinc levels, and were normalized two weeks after zinc supplementation.[45]

Zinc, as a trace mineral, is present in the cerebral cortex, pineal gland, and hippocampus where it acts as an atypical neuromodulator.[46][47][48] In the hippocampus, particularly the vesicles of mossy fibers, zinc can reach concentrations of 220-300M which is around 8% of total brain zinc[49] (concentrations of free zinc are more modest at 1-20M[50][51]) and is sensitive to prolonged (but not acute) zinc deficiency,[52] while in the pineal gland it may regulate the response of this organ to leptin.[53]

Similar to most neuromodulators, zinc is released from the synapse upon action potentials.[54]

The cell can take up zinc via ion channels such as the AMPK/kainate calcium channel (in neurons)[55] where it is then taken up by the cell's mitochondria.[55][56]

The zinc ion has been noted to possess moderate potency NMDA receptor inhibitory actions in the range of 100-1,000M without affecting basal currents, while the activity of 10M was weak and the IC50 value placed near 100M;[57] the effects on NMDA receptor agonists appeared to be similar to magnesium.[57]

Zinc may also activate neuronal potassium channels and reduce glutamate release into the synapse.[58]

In the corpus callosum (commissure between brain hemispheres, function appears to be altered in depression[59][60] and serotonin uptake may be hindered by antidepressants fluoxetine and imipramine[61]), elemental zinc and zinc sulfate can enhance uptake at a relevant concentration of 1M by 45%.[62] This increase in uptake was also noted the cingulate cortex (58%) and Raphe nucleus (65%), concentrations of zinc between 10-100nM were ineffective, and the hindering effects of antidepressants on this function was negated with 1M zinc.[62]

Brain-derived neurotrophic factor (BDNF) is a protein found in both serum and brain (serum concentrations thought to be reflective of brain concentrations[63]) which is involved in regulating neuronal growth and plasticity;[64] BDNF signalling is implicated in both depression and memory function.[65] Zinc is known to be involved with BDNF as a deficiency of zinc seems to reduce the ability of BDNF in activating its receptors[66] and zinc itself can form a complex with the BDNF protein,[67] although it is primarily thought that via activating some metalloprotein enzymes (MMP-2 and MMP-9) which has been noted with oral zinc in mice[68] that zinc helps cleave the inactive form of BDNF (pro-BDNF) into 'mature' or active BDNF.[69]

High levels of dietary zinc in mice (30ppm via diet with 60ppm via supplemented drinking water) has been noted to reduce the actions of BDNF in the brain and impair memory, which was noted to be associated with a zinc deficiency in the hippocampus.[70] Zinc injections directly increase BDNF,[70] and the reason why high oral intake led to a reduction in hippocampal zinc is not known.

The antidepressive effects of zinc are thought to be mediated by an increase in BDNF, which has been noted in the serum of depressed humans given 30mg elemental zinc over the course of 12 weeks compared to placebo.[71] This study noted that baseline BDNF in serum, 15.37+/-8.28ng/mL, was increased 42% to reach 21.84+/-6.87ng/mL despite no change in placebo and this occurred alongside a 41% increase in serum zinc concentrations.[71]

Such an increase in BDNF has failed to occur elsewhere when 25mg was given as adjuvant over the same time length to depressed persons already on SSRI therapy despite zinc bettering symptoms of depression.[72]

Despite its importance in the brain, high concentrations of zinc can be excitotoxic[73] and this is sometimes seen in ischemic injury where an excess amount of zinc is released from the synapse and mediates cell death[73][74] and infarctions.[75] This is why zinc chelators are therapeutic in instances of stroke rehabilitation.[76]

Obsessive compulsive disorder is known to at least be associated with glutaminergic abnormalities, particular an excessive level of synaptic glutamate and signalling thereof[77][78] which positively correlates with symptom severity.[79] As glutamate antagonists have been previously implicated in treating OCD[80] and zinc has the potential to be anti-glutaminergic, it is investigated for possible benefits.

The addition of zinc (220mg twice daily) to fluoxetine therapy (20mg) for obsessive compulsive disorder is able to reduce symptoms of OCD as assessed by the Y-BOCS rating scale, although the benefits were present at weeks two and eight but not 4-6.[81]

A deficiency of zinc is known to be a cause of anorexia (reduction of appetite, not the same as anorexia nervosa), and is usually the first symptom of a zinc deficiency[82] and is shortly followed by depressive symptoms and anhedonia.[83]

In rats, orally supplemented zinc (19mcg/kg) appears to stimulate food intake and this effect was not observed with other bivalent cations.[84] Injections of zinc seem ineffective,[84] even in deficient rats.[85]

Oral zinc appears to stimulate the vagal nerve (effects abolished by vagotomy[84]) which then increase mRNA translation of the two appetite stimulating neural factors orexin and neuropeptide Y (also abolished by antagonists of these receptors[84]). Zinc is known to activate the GPR39 receptor (a Ghrelin receptor)[86] and since ghrelin is known to stimulate these two neural fators via the vagus nerve[87][88] it is thought that this receptor is the molecular target of zinc.

In children with ADHD, 30mg elemental zinc daily for 13 weeks (final five weeks used alongside D-amphetamine) was able to reduce the amount of D-amphetamine that was needed by 37% and reduced affective blunting from 21% (placebo with amphetamine) to 11%; however, zinc supplementation inherently failed to benefit symptoms of ADHD.[89]

Depressed patients appear to have reduced circulating zinc concentrations in serum[90] which is further reduced in treatment resistant persons relative to treatment non-resistant (treatment being imipramine)[91] and the magnitude of zinc deficiency correlating with severity of depression.[92][93] Overall, persons with depression seem to usually have lower zinc concentrations in serum and the worse the symptoms of depression the lower the zinc concentration tends to be.

At least in rats, the depressive[94] and behavioural symptoms (increased susceptability to stress[95]) that are seen with two weeks of zinc deprivation are normalized upon supplemetnation of zinc. Interestingly, deprivation of zinc causes rats to be resistant to fluoxetine (SSRI) therapy.[94]

In patients with major depression given zinc therapy (25mg elemental zinc) alongside their antidepressant medication (SSRIs) noted that supplementation had an adjuvant role by reducing depressive symptoms over 12 weeks when compared to SSRI paired with placebo;[72] monotherapy alone at 30mg elemental zinc in overweight/obese depressed persons appears to also reduce depressive symptoms (assessed by BDI II) over 12 weeks when compared to placebo.[71]

Zinc has been reported to noncompetitively inhibit glycogen synthase kinase-3 (GSK3) with an IC50 of 15M.[96] As GSK3 is a molecular target of mood disorders[97] and mood disorders being associated with alterations in zinc metabolism[98] supplementation is thought to have a potential role in its treatment.[17]

In otherwise healthy young women given 7mg of elemental zinc in a multivitamin format (placebo given the same multivitamin), depressive and aggressive symptoms were modestly but significantly reduced relative to placebo.[99] This modest benefit to mood has failed to occur in healthy elderly perosns (70-87yrs) given 15-30mg zinc as assessed by POMS.[100]

In persons given imipramine but were resistant to treatment, supplementation of 25mg elemental zinc for twelve weeks is able to reduce depressive symptoms relative to placebo to the levels seen with non-resistant persons as assessed by BDI, HAMD, and CGI.[101]

Zinc is known to be highly concentrated in the hippocampus[46][49] and a deficiency of zinc is associated with both mood disorders as well as impaired memory formation.[102] While a dietary insufficiency of zinc is known to cause a corresponding decrease in hippocampal zinc (attenuated with supplemental zinc[102]), high oral intakes in mice (additional 60ppm to drinking water) have also been noted to paradoxically reduce zinc concentrations in the hippocampus[70] which is not seem with mild elevations in rats (10ppm).[103]

The negative effects of low zinc concentrations in the hippocampus seem to be related to spatial memory,[102] and spatial memory is known to be associated with brain-derived neurotrophic factor (BDNF) signalling;[104] accordingly, injections of zinc into the rat brain cause dose-dependent increases in BDNF signalling and protein content[70] and a deficiency results in decreased BDNF signalling although the elevated protein content suggests insensitivity of the TrkB receptor.[66]

In general and in studies on how zinc influences spatial memory formation, low dose zinc in drinking water (10ppm) has been associated with beneficial,[68][105] adverse,[103] and no significant alterations.[70] Greater elevations (60ppm) have been noted to force a reduction in spatial learning associated with reduced hippocampal zinc and BDNF,[70] although at least one study noted impairments in memory at 10ppm alongside an increase in brain zinc concentrations.[103] This negative effect of zinc on spatial memory has been noted in one rat study to be significantly reduced with coadministration of copper (at approximately 2.5% the dose of zinc).[106]

In persons who experienced subacute stroke and had suboptimal dietary intake of zinc (6.6mg or less), supplementation of 10mg elemental zinc was associated with greater improvements than placebo on cognition as assessed by the NIH stroke scale after 30 days.[107]

Zinc is thought to be an anti-artherogenic agent[108] and in particular a zinc deficiency is thought to be a risk factor for artherogenesis with supplementation alleviating this risk.[109] Dietary zinc intake is known to be inversely associated with artherosclerotic buildup in arteries.[110]

In otherwise healthy elderly persons (higher risk of zinc deficiency), supplementation of 45mg elemental zinc daily (as gluconate) daily for six months is associated with reductions in cell adhesion factors (ICAM-1 and vCAM-1) and inflammatory cytokines including C-reactive protein, IL-6, and MCP-1.[111]

Supplementation of 20mg elemental zinc in obese insulin resistant children over eight weeks is associated with a reduction in total cholesterol and LDL-C.[112]

Oxidized LDL-C appears to be reduced when insulin resistant children are given 20mg elemental zinc for eight weeks, possibly secondary to reducing the state of insulin resistance.[112]

20M zinc has been noted to, in vitro in liver cells, to increase the activity of glycogen synthase 2-fold secondary to its inhibition of GSK-3 (IC50 15M).[96]

Zinc has been reported to act via the insulin receptor[113] and phosphorylate Akt in vitro, which is downstream of the insulin receptor.[30] The inhibition of glycogen synthase kinase-3 (GSK3) that occurs with zinc[96] is able to preserve insulin signalling, as GSK3 is a negative regulator of insulin signalling via IRS-1.[114] Zinc can augment uptake of glucose into cells that express insulin-sensitive GLUT4, but not other GLUT transporters.[96]

In diabetic individuals (following information seems to apply equally to type I and type II diabetics), urinary zinc excretion rates are increased[25][26][27] and although serum zinc concentrations are unreliably influenced (increased,[25][28] decreased,[29][30][31] or not different from non-diabetic controls[32]) cellular concentrations of zinc as measured in immune cells (mononuclear cells, granulocytes, lymphocytes and leucocytes) tend to be reduced relative to nondiabetic controls.[29][33][30]

Beyond measuring zinc concentrations themselves (as serum markers are not thought to be overly reliable for subclinical deficiencies[115]), a sensitive biomarker for zinc deficiency (Ecto 5' nucleotidase[116]) is also known to be reduced in diabetic persons relative to control.[117]

Three weeks of supplementation with 30mg elemental zinc (glycine chelation) appears to be sufficient to at least partially restore a zinc deficiency in diabetics.[117]

In obese insulin resistant children (who were likely deficient in zinc) given 20mg elemental zinc for eight weeks supplementation was associated with a betterment of all biomarkers of glucose metabolism including blood glucose (7% reduction), fasting insulin (23% reduction), and insulin sensitivity as assessed by HOMA-IR (31% improvement)[112] which has been reported elsewhere in a replication.[118]

In diabetics who have been confirmed to have adequate stores of zinc, further supplementation of high dose zinc (240mg elemental zinc as gluconate) for three months has failed to have any appreciable benefit.[119]

Tumor necrosis factor alpha (TNF-) is a cytokine that is reduced in states of zinc deficiency (restored upon zinc replenishment[120]).

Ex vivo production of TNF from macrophages in elderly persons who supplemented 45mg elemental zinc for a year appears to be reduced.[121]

IL-2 is known to be decreased with zinc deficiency[120] and restored upon replenishment.[120]

Ex vivo production of IL-2 (assessed by the induction of IL-2 mRNA from stimulated immune cells) is increased with supplementation of zinc at 45mg for a year, despite basal concentrations of IL-2 being unaffected.[121]

Zinc deficiency is known to lead to a reduced count of T-cells and subsequently depressed humoral and cell-mediated immunity.[122]

A meta-analysis of 15 trials including 1360 persons overall noted that zinc, in the form of lozenges (gluconate) or syrup (sulfate), was associated with less duration and severity of the common cold when taken within 24 hours of onset that, after a week, had an odds ratio of 0.45 (less than half the risk).[123]

Supplementation of 45mg zinc in elderly persons (with lower zinc concentrations in serum relative to young controls) for a year is associated with a reduced rate of upper respiratory tract infections (50% reduction that failed to be significant) and general infections (88% occurrence reduced to 29%).[121]

Prolonged supplementation of zinc over five months is associated with a reduced incidence of sickness (RR 0.64) although with a high variability.[123]

In children with acute pneumonia, 10-20mg elemental zinc (as acetate syrup) over two weeks failed to outperform placebo in reducing the length of sickness.[124]

Supplementation of zinc at 20mg as adjuvant therapy (alongside antibiotics) was effective in further reducing recovery time in children under two years old with very severe pneumonia, but due to having no effect in severe pneumonia and the benefit in very severe being lost when controlling for underweight children the authors concluded no significant overall effect of treatment.[125] Other studies using the same dose that differentiate between severe and nonsevere pneumonia note a failure of zinc therapy outright relative to placebo[126][127][128] or that the beneficial effects were insignificant (statistically and clinically).[129] Although most evidence suggests a lack of efficacy, there is some counter evidence with the same protocol noting efficacy in reducing the length of sickness for severe pneumonia[130] and a study that noted a failure overall with zinc supplementation did report reduced mortality with severe pneumonia (which mostly protected children with HIV).[128]

The usage of zinc as a preventative for two weeks (10-20mg elemental zinc daily) was unable to influence the occurrence of pneumonia in children measured over the following six months.[131]

Adults with diagnosed HIV appear to be at greater relative risk for zinc deficiencies at up to 50%[132][133][134] and those who are deficient seem to have faster disease progression[135][136] and mortality;[137] a dietary surplus of zinc also appears to be associated with negative effects in this cohort, specifically an increased disease progression rate to AIDS.[138]

In HIV positive adults with confirmed low plasma zinc concentrations (0.75g/mL or less) given 12-15mg elemental zinc daily for 18 months, zinc supplementation was associated with a four-fold reduced risk of immunological failure relative to placebo without affecting viral load[139] and has elsewhere been associated with significantly less opportunistic infections regardless of whether or not subjects were on antiretroviral therapy.[140]

In children diagnosed with HIV who also experience severe pneumonia, supplementation of zinc appears to be effective in reducing mortality (7 deaths in control and none noted with zinc at 20mg daily for seven days).[128]

In a study dividing athletes and sedentary persons into a zinc supplement (5mg/kg zinc sulfate daily), both athletic and sedentary persons given zinc experienced a reduction in levels of lipid peroxidation relative to placebo and an increase in levels of the enzymes glutathione peroxidase and SOD.[141]

Bodily zinc stores are positively associated with serum testosterone[142][143] and increased urinary excretion negatively associated (as well as magnesium).[144]

Zinc deficiency is also associated with an impairment of converting cholesterol and lipid precursors into sex hormones despite testicular cell uptake being unaffected[145] and other side-effects associated with zinc deficiency include the population of androgen receptors being reduced overall (59% of control)[146] and in male sex organs (36% of control);[147] this may be related to how the androgen receptors have a zinc binding site,[148] and their functionality is impaired without adequate zinc.

When looking at rat studies that are not models of deficiency, zinc supplementation is able to increase circulating testosterone and free testosterone when injected at 3mg/kg[149] and oral intake of 20mg/kg zinc chloride has increased testosterone to levels higher than baseline in rats.[150]

In human studies of zinc deficiency supplementation of zinc is able to increase circulating testosterone concentrations, with this study noting that 250mg zinc sulfate for six weeks is able to increase testosterone by 84% (1.55nM/dL to 2.96nM/dL) in persons on hemodialysis.[151]

Infertile men who also have low testosterone (less than 4.8ng/mL) experience an increase in testosterone following zinc supplementation, but this is not observed in men with normal testosterone levels.[152]

Supplementation of ZMA in persons with an adequate zinc intake in the diet (11.9-23.2mg) failed to significantly increase circulating testosterone or free testosterone[1] and this failure to increase basal testosterone concentrations is also seen with 15mg elemental zinc in cyclists[153] and 3mg/kg zinc sulfate in elite wrestlers.[154]

When measuring testosterone acutely following exercise, there is a slight increase in free testosterone associated with zinc supplementation at 15mg in men who are not otherwise deficient[153] and the decrease in testosterone and free testosterone that may occur with exhaustive exercise is attenuated with zinc sulphate supplementation at 3mg/kg in elite wrestlers[154] and in sedentary men subject to cycling.[155]

Zinc is thought to reduce DHT secondary to inhibition of 5-reductase (converts testosterone to DHT) in the 3-15mM range (up to 98% inhibition), although concentrations as low as 500M are minimially effective (30%).[156] It is synergistic with vitamin B6 in this regard despite B6 not possessing any inherent inhibitory properties, which may explain the formulation of ZMA.

Injections of 10-20mg zinc (gluconate and arginine included in the weights here) into the prostate of rats has noted inhibitory effects on 5-reductase (50.48% at 20mg)[157] although a study in human prostate tissue in vitro noted that low concentrations (300nM) increased activity of this enzyme while higher concentrations (3mM) were potently inhibitory.[158]

When looking at the subdivisions of 5-reductase, the type I variant is effectively inhibited in skin cells with an IC50 of 2M while it is fairly ineffective on type II[159] and in these tissues it is still synergistic with B6.[156]

In infertile men, regardless of whether circulating testosterone was above or below the predetermined threshold (4.8ng/mL) supplemental zinc was able to increase circulating concentrations of DHT.[152]

A zinc deficiency in rats is associated with an increased expression of estrogen receptors (57%)[146]

IGF-1[160][117] and IGFBP3[160] are reduced in persons experiencing a dietary zinc deficiency, which is normalized upon supplementation.

An increase in IGF-1 has been noted in elderly persons given 30mg zinc supplementation daily for four weeks, where the 22.4+/-4.7% increase seen with a whey protein supplement was boosted to 48.2+/-14%.[161]

Leptin is known to interact with zinc at the level of the pineal gland[53] and may mediate its actions.[162] A zinc deficiency is known to reduce leptin production and secretion from adipocytes[163] which has been detected in rats[164] and humans.[120]

Leptin secretion can be positively influenced by insulin[165] although as zinc repletion does not influence insulin[120] this is not thought to be a mechanism of action. TNF- and interleukin-2 (IL-2) have both been found to be increased when a zinc deficient person has their zinc status restored[120] and these factors are known to induce leptin expression.[166] IL-2 itself is zinc dependent,[167] and it is thought that the influence on leptin couldl also be indirect via these two molecules.

In men with marginal zinc deficiency (restricted to about 5mg daily for 4+/-2 months), supplementation of 30-60mg elemental zinc (as acetate) daily for 6-12 weeks is associated with a 64% increase in leptin relative to the deficient state.[120]

Reductions in taste acuity are among the first noticeable signs of zinc deficiency, usually alongside anorexia (loss of appetite) and impairment in cognition.[168] This is likely because of a zinc-dependent enzyme, gustin, being reduced in activity when salivary zinc is low[169] and this condition is easily treated with supplemental zinc.[170]

Adolescents given zinc supplements over the course of ten weeks have been noted to experience increases in taste acuity as assessed by recognition thresholds for salt was improved;[171] these subjects (adolescent girls in India) usually have zinc deficiency rates around 58.3-65%[172][173] and thus the observed effects could be from normalizing a deficiency.

Loss of taste associated with chemotherapy does not appear to be rehabilitated with supplementation of 220mg zinc sulfate (50mg elemental zinc) twice daily.[174]

In low socioeconomic children at risk for zinc deficiency, 15mg elemental zinc daily for ten weeks is associated with reduced plaque formation on teeth.[175]

Zinc chloride appears to be capable of preventing secretagogue-induced acid secretion in rat and human stomach tissue,[176] which although therapeutic for the stomach may limit its own subsequent absorption.[177]

Trace minerals appear to be altered in their concentrations in the cirrhotic liver and serum, with a known decrease in zinc[178][179] and increase in copper[179][180] relative to healthy controls; the deficiency in zinc appears to positively correlate with disease progression.[181]

In persons with liver cirrhosis, supplementation of 50mg elemental zinc (as sulfate) daily for 90 days is associated with improvements in cirrhotic state as assessed by Child-Pugh score (6.56 down to 5.72; 13% improvement) which was associated with less bodily copper levels.[182]

Very high levels of zinc intake (330mg daily) has been implicated in alleviating leaky gut syndrome in those with Crohn's Disease.[183] It can also prevent or alleviate damage to the intestinal mucosa and some to the liver done by alcohol[184][185][186] and due to alcohol causing zinc depletion, can also provide therapeutic-like benefit in treating alcohol-induced damage to the gut and liver.[187][188] Many of these effects were noted as dose dependent, but were seen at 3-5mg/kg bodyweight (an incredibly high dose).

Zinc deficiency is associated with impaired hearing in mice and rats, which is normalized upon consuming enough dietary levels of zinc.[189][190] This may be related to relatively high concentrations of zinc in some ear structures (cochlea and vestibule) where it exerts protective effects from stessors[191] possibly related to its role as a neuromodulator or as a component of Cu/Zn superoxide dismutase;[192] the latter of which is known to be protective of hearing.[193]

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Zinc - Scientific Review on Usage, Dosage, Side Effects ...

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Nov 16th, 2018 | Filed under Testosterone